American Diabetes Association

Standards of
Medical Care in
Diabetesd2015
January 2015 Volume 38, Supplement 1

[T]he simple word Care may suffice to express [the journal’s] philosophical
mission. The new journal is designed to promote better patient care by
serving the expanded needs of all health professionals committed to the care
of patients with diabetes. As such, the American Diabetes Association views
Diabetes Care as a reaffirmation of Francis Weld Peabody’s contention that
“the secret of the care of the patient is in caring for the patient.”
—Norbert Freinkel, Diabetes Care, January-February 1978
EDITOR IN CHIEF

William T. Cefalu, MD

ASSOCIATE EDITORS EDITORIAL BOARD

George Bakris, MD Nicola Abate, MD Rory J. McCrimmon, MBChB, MD, FRCP

Lawrence Blonde, MD, FACP Silva Arslanian, MD Harold David McIntyre, MD, FRACP
Andrew J.M. Boulton, MD Angelo Avogaro, MD, PhD Sunder Mudaliar, MD
Mary de Groot, PhD Ananda Basu, MD, FRCP Gianluca Perseghin, MD
Eddie L. Greene, MD John B. Buse, MD, PhD Anne L. Peters, MD
Robert Henry, MD Sonia Caprio, MD Jonathan Q. Purnell, MD
Sherita Hill Golden, MD, MHS, FAHA Robert Chilton, DO Peter Reaven, MD
Frank Hu, MD, MPH, PhD Kenneth Cusi, MD, FACP, FACE Helena Wachslicht Rodbard, MD
Derek LeRoith, MD, PhD Paresh Dandona, MD, PhD Pedro Romero-Aroca, PhD
Robert G. Moses, MD Stefano Del Prato, MD David J. Schneider, MD
Stephen Rich, PhD Dariush Elahi, PhD Elizabeth R. Seaquist, MD
Matthew C. Riddle, MD Franco Folli, MD, PhD Norbert Stefan, MD
Julio Rosenstock, MD Robert G. Frykberg, DPM, MPH Jeff Unger, MD
William V. Tamborlane, MD W. Timothy Garvey, MD Ram Weiss, MD, PhD
Katie Weinger, EdD, RN Ronald B. Goldberg, MD Deborah J. Wexler, MD, MSc
Judith Wylie-Rosett, EdD, RD Margaret Grey, DrPH, RN, FAAN Joseph Wolfsdorf, MD, BCh
Richard Hellman, MD Tien Yin Wong, MBBS, FRCSE, FRANZCO,
Rita Rastogi Kalyani, MD, MHS, FACP MPH, PhD

AMERICAN DIABETES ASSOCIATION OFFICERS

CHAIR OF THE BOARD PRESIDENT-ELECT, MEDICINE & SCIENCE
Janel L. Wright, JD Desmond Schatz, MD
PRESIDENT, MEDICINE & SCIENCE PRESIDENT-ELECT, HEALTH CARE &
Samuel Dagogo-Jack, MD, FRCP EDUCATION
Margaret Powers, PhD, RD, CDE
PRESIDENT, HEALTH CARE & EDUCATION
David G. Marrero, PhD SECRETARY/TREASURER-ELECT
Lorrie Welker Liang
SECRETARY/TREASURER
Richard Farber, MBA INTERIM CHIEF EXECUTIVE OFFICER
Suzanne Berry, MBA, CAE
CHAIR OF THE BOARD-ELECT
Robin J. Richardson CHIEF SCIENTIFIC & MEDICAL OFFICER
Robert E. Ratner, MD, FACP, FACE

The mission of the American Diabetes Association

is to prevent and cure diabetes and to improve
the lives of all people affected by diabetes.
 Diabetes Care is a journal for the health care practitioner that is intended to
increase knowledge, stimulate research, and promote better management of people
with diabetes. To achieve these goals, the journal publishes original research on
human studies in the following categories: Clinical Care/Education/Nutrition/
Psychosocial Research, Epidemiology/Health Services Research, Emerging
Technologies and Therapeutics, Pathophysiology/Complications, and Cardiovascular
and Metabolic Risk. The journal also publishes ADA statements, consensus reports,
clinically relevant review articles, letters to the editor, and health/medical news or points
of view. Topics covered are of interest to clinically oriented physicians, researchers,
epidemiologists, psychologists, diabetes educators, and other health professionals.
More information about the journal can be found online at care.diabetesjournals.org.
Diabetes Care (print ISSN 0149-5992, online ISSN 1935-5548) is owned, controlled, and
published monthly by the American Diabetes Association, Inc., 1701 North Beauregard St.,
Alexandria, VA 22311. Diabetes Care is a registered trademark of the American Diabetes
Association.
Copyright © 2015 by the American Diabetes Association, Inc. All rights reserved. Printed in
the USA. Requests for permission to reuse content should be sent to Copyright Clearance
Center at www.copyright.com or 222 Rosewood Dr., Danvers, MA 01923; phone: (978)
750-8400; fax: (978) 646-8600. Requests for permission to translate should be sent to
Permissions Editor, American Diabetes Association, at permissions@diabetes.org.
The American Diabetes Association reserves the right to reject any advertisement for
any reason, which need not be disclosed to the party submitting the advertisement.
Commercial reprint orders should be directed to Sheridan Content Services,
(800) 635-7181, ext. 8065.
Single issues of Diabetes Care can be ordered by calling toll-free (800) 232-3472, 8:30 A.M.
to 5:00 P.M. EST, Monday through Friday. Outside the United States, call (703) 549-1500.
Rates: $75 in the United States, $95 in Canada and Mexico, and $125 for all other countries.
Diabetes Care is available online at care.diabetesjournals.org. Please call the
numbers listed above, e-mail membership@diabetes.org, or visit the online journal for
more information about submitting manuscripts, publication charges, ordering reprints,
subscribing to the journal, becoming an ADA member, advertising, permission to reuse
content, and the journal’s publication policies.
Periodicals postage paid at Alexandria, VA, and additional mailing offices.
POSTMASTER: Send address changes to Diabetes Care, American Diabetes Association, Inc.,
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PRINTED IN THE USA of charge only when losses have been sustained in transit and when the reserve stock permits.

AMERICAN DIABETES ASSOCIATION PERSONNEL AND CONTACTS

EDITORIAL OFFICE DIRECTOR EDITORIAL MANAGERS MANAGING DIRECTOR, MEDIA SALES
Lyn Reynolds Valentina Such Clare Liberis
Nancy C. Baldino cliberis@diabetes.org
PEER REVIEW MANAGER
212-725-4925, ext. 3448
Shannon Potts PRODUCTION MANAGER
ASSOCIATE DIRECTOR, BILLING & COLLECTIONS
EDITORIAL ASSISTANT Amy S. Gavin
Laurie Ann Hall
Rita Summers
TECHNICAL EDITOR DIRECTOR, MEMBERSHIP/SUBSCRIPTION
EDITORIAL OFFICE SECRETARIES Oedipa Rice SERVICES
Raquel Castillo Donald Crowl
Joan Garrett VICE PRESIDENT, CORPORATE ALLIANCES ADVERTISING REPRESENTATIVES
Nancy Stinson Harris The Jackson-Gaeta Group, Inc.
MANAGING DIRECTOR, SCHOLARLY
JOURNAL PUBLISHING
B. Joseph Jackson
ADVERTISING MANAGER bartjack@aol.com
Christian S. Kohler
Julie DeVoss Graff Paul Nalbandian
DIRECTOR, SCHOLARLY JOURNAL PUBLISHING jdevoss@diabetes.org pnalbandian4ada@aol.com
Heather L. Norton (703) 299-5511 (973) 403-7677
 January 2015 Volume 38, Supplement 1

Standards of Medical Care in Diabetes—2015

S1 Introduction S49 8. Cardiovascular Disease and Risk Management
S3 Professional Practice Committee Hypertension/Blood Pressure Control
Dyslipidemia/Lipid Management
S4 Standards of Medical Care in Diabetes—2015: Antiplatelet Agents
Summary of Revisions Coronary Heart Disease
S5 1. Strategies for Improving Care
S58 9. Microvascular Complications and Foot Care
Diabetes Care Concepts
Care Delivery Systems Nephropathy
When Treatment Goals Are Not Met Retinopathy
Neuropathy
S8 2. Classification and Diagnosis of Diabetes Foot Care
Classification S67 10. Older Adults
Diagnostic Tests for Diabetes
Categories of Increased Risk for Diabetes Treatment Goals
(Prediabetes) Hypoglycemia
Type 1 Diabetes Pharmacological Therapy
Type 2 Diabetes S70 11. Children and Adolescents
Gestational Diabetes Mellitus
Monogenic Diabetes Syndromes Type 1 Diabetes
Cystic Fibrosis–Related Diabetes Type 2 Diabetes
Psychosocial Issues
S17 3. Initial Evaluation and Diabetes Management
Planning S77 12. Management of Diabetes in Pregnancy
Medical Evaluation Diabetes in Pregnancy
Management Plan Preconception Counseling
Common Comorbid Conditions Glycemic Targets in Pregnancy
S20 4. Foundations of Care: Education, Nutrition, Pregnancy and Antihypertensive Drugs
Physical Activity, Smoking Cessation, Management of Gestational Diabetes Mellitus
Psychosocial Care, and Immunization Management of Pregestational Type 1 Diabetes
and Type 2 Diabetes in Pregnancy
Diabetes Self-management Education and Support Postpartum Care
Medical Nutrition Therapy
Physical Activity S80 13. Diabetes Care in the Hospital, Nursing Home,
Smoking Cessation and Skilled Nursing Facility
Psychosocial Assessment and Care Hyperglycemia in the Hospital
Immunization Glycemic Targets in Hospitalized Patients
S31 5. Prevention or Delay of Type 2 Diabetes Antihyperglycemic Agents in Hospitalized Patients
Preventing Hypoglycemia
Lifestyle Modifications Diabetes Care Providers in the Hospital
Pharmacological Interventions Self-management in the Hospital
Diabetes Self-management Education and Support Medical Nutrition Therapy in the Hospital
S33 6. Glycemic Targets Bedside Blood Glucose Monitoring
Discharge Planning
Assessment of Glycemic Control Diabetes Self-management Education
A1C Goals
Hypoglycemia S86 14. Diabetes Advocacy
Intercurrent Illness
Advocacy Position Statements
S41 7. Approaches to Glycemic Treatment
S88 Professional Practice Committee for the Standards
Pharmacological Therapy for Type 1 Diabetes of Medical Care in Diabetes—2015
Pharmacological Therapy for Type 2 Diabetes
Bariatric Surgery S90 Index

This issue is freely accessible online at care.diabetesjournals.org.

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Diabetes Care Volume 38, Supplement 1, January 2015
Introduction
Diabetes Care 2015;38(Suppl. 1):S1–S2 | DOI: 10.2337/dc15-S001
Diabetes is a complex, chronic illness re-
quiring continuous medical care with
multifactorial risk-reduction strategies
beyond glycemic control. Ongoing pa-
tient self-management education and
support are critical to preventing acute
complications and reducing the risk of
long-term complications. Significant
evidence exists that supports a range
of interventions to improve diabetes
outcomes.
The American Diabetes Association’s
(ADA’s) “Standards of Medical Care in
Diabetes” is intended to provide cli-
nicians, patients, researchers, payers,
and other interested individuals with
the components of diabetes care, gen-
eral treatment goals, and tools to eval-
uate the quality of care. The Standards
of Care recommendations are not in-
tended to preclude clinical judgment
and must be applied in the context of
excellent clinical care, with adjustments
for individual preferences, comorbid-
ities, and other patient factors. For
more detailed information about man-
agement of diabetes, please refer to
Medical Management of Type 1 Diabetes
(1) and Medical Management of Type 2
Diabetes (2).
The recommendations include screen-
ing, diagnostic, and therapeutic actions
that are known or believed to favor-
ably affect health outcomes of patients
with diabetes. Many of these interven-
tions have also been shown to be cost-
effective (3).
The ADA strives to improve and update
the Standards of Care to ensure that clini-
cians, health plans, and policy makers can
continue to rely on them as the most au-
thoritative and current guidelines for di-
abetes care.
“Standards of Medical Care in Diabetes” was originally approved in 1988. Most recent review/revision: October 2014.
© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit,
and the work is not altered.
ADA STANDARDS, STATEMENTS,
AND REPORTS
The ADA has been actively involved in
the development and dissemination of
diabetes care standards, guidelines, and
related documents for over 20 years.
ADA’s clinical practice recommenda-
tions are viewed as important resources
for health care professionals who care
for people with diabetes. ADA’s “Stan-
dards of Medical Care in Diabetes,”
position statements, and scientific
statements undergo a formal review
process by ADA’s Professional Practice
Committee (PPC) and the Executive
Committee of the Board of Directors.
The Standards and all ADA position state-
ments, scientific statements, and consensus
reports are available on the Association’s
Web site at http://professional.diabetes.org/
adastatements.
“Standards of Medical Care in Diabetes”
Standards of Care: ADA position state-
ment that provides key clinical practice
recommendations. The PPC performs an
extensive literature search and updates
the Standards annually based on the
quality of new evidence.
ADA Position Statement
A position statement is an official ADA
point of view or belief that contains clinical
or research recommendations. Position
statements are issued on scientific or med-
ical issues related to diabetes. They are
published in ADA journals and other scien-
tific/medical publications. ADA position
statements are typically based on a sys-
tematic review or other review of pub-
lished literature. Position statements
undergo a formal review process. They
are updated annually or as needed.
S1
INTRODUCTION
ADA Scientific Statement
A scientific statement is an official
ADA point of view or belief that may or
may not contain clinical or research rec-
ommendations. Scientific statements
contain scholarly synopsis of a topic re-
lated to diabetes. Workgroup reports
fall into this category. Scientific state-
ments are published in the ADA journals
and other scientific/medical publications,
as appropriate. Scientific statements also
undergo a formal review process.
Consensus Report
A consensus report contains a compre-
hensive examination by an expert panel
(i.e., consensus panel) of a scientific or
medical issue related to diabetes. A con-
sensus report is not an ADA position and
represents expert opinion only. The cat-
egory may also include task force and
expert committee reports. The need
for a consensus report arises when clini-
cians or scientists desire guidance on
a subject for which the evidence is con-
tradictory or incomplete. A consensus
report is typically developed immedi-
ately following a consensus conference
where the controversial issue is exten-
sively discussed. The report represents
the panel’s collective analysis, evalua-
tion, and opinion at that point in time
based in part on the conference pro-
ceedings. A consensus report does not
undergo a formal ADA review process.
GRADING OF SCIENTIFIC EVIDENCE
Since the ADA first began publishing
practice guidelines, there has been con-
siderable evolution in the evaluation of
scientific evidence and in the develop-
ment of evidence-based guidelines.
In 2002, we developed a classification
S2 Introduction
Table 1—ADA evidence-grading system for “Standards of Medical Care in Diabetes”
Level of
evidence Description
A Clear evidence from well-conducted, generalizable randomized controlled
trials that are adequately powered, including
c Evidence from a well-conducted multicenter trial
c Evidence from a meta-analysis that incorporated quality ratings in the
analysis
Compelling nonexperimental evidence; i.e., “all or none” rule developed by
the Centre for Evidence-Based Medicine at the University of Oxford
Supportive evidence from well-conducted randomized controlled trials that
are adequately powered, including
c Evidence from a well-conducted trial at one or more institutions
c Evidence from a meta-analysis that incorporated quality ratings in the
analysis
B Supportive evidence from well-conducted cohort studies
c Evidence from a well-conducted prospective cohort study or registry
c Evidence from a well-conducted meta-analysis of cohort studies
Supportive evidence from a well-conducted case-control study
C Supportive evidence from poorly controlled or uncontrolled studies
c Evidence from randomized clinical trials with one or more major or three
or more minor methodological flaws that could invalidate the results
c Evidence from observational studies with high potential for bias (such as
case series with comparison with historical controls)
c Evidence from case series or case reports
Conflicting evidence with the weight of evidence supporting the
recommendation
E Expert consensus or clinical experience
system to grade the quality of scienti- and codify the evidence that forms the
fic evidence supporting ADA recommen- basis for the recommendations.
dations for all new and revised ADA ADA recommendations are assigned
position statements. A recent analysis ratings of A, B, or C, depending on the
of the evidence cited in the Standards quality of evidence. Expert opinion E is a
of Care found steady improvement in separate category for recommendations
quality over the past 10 years, with last in which there is no evidence from clin-
year’s Standards for the first time having ical trials, in which clinical trials may
the majority of bulleted recommenda- be impractical, or in which there is con-
tions supported by A- or B-level evi- flicting evidence. Recommendations
dence (4). A grading system (Table 1) with an A rating are based on large
developed by ADA and modeled after well-designed clinical trials or well-
existing methods was used to clarify done meta-analyses. Generally, these
Diabetes Care Volume 38, Supplement 1, January 2015
recommendations have the best chance
of improving outcomes when applied to
the population to which they are appro-
priate. Recommendations with lower
levels of evidence may be equally impor-
tant but are not as well supported.
Of course, evidence is only one com-
ponent of clinical decision making. Clini-
cians care for patients, not populations;
guidelines must always be interpreted
with the individual patient in mind.
Individual circumstances, such as co-
morbid and coexisting diseases, age, ed-
ucation, disability, and, above all,
patients’ values and preferences, must
be considered and may lead to different
treatment targets and strategies. Also,
conventional evidence hierarchies, such
as the one adapted by the ADA, may
miss nuances important in diabetes
care. For example, although there is ex-
cellent evidence from clinical trials sup-
porting the importance of achieving
multiple risk factor control, the optimal
way to achieve this result is less clear. It
is difficult to assess each component of
such a complex intervention.
References
1. Kaufman FR (Ed.). Medical Management of
Type 1 Diabetes, 6th ed. Alexandria, VA, Amer-
ican Diabetes Association, 2012
2. Burant CF (Ed.). Medical Management of
Type 2 Diabetes, 7th ed. Alexandria, VA, Amer-
ican Diabetes Association, 2012
3. Li R, Zhang P, Barker LE, Chowdhury FM,
Zhang X. Cost-effectiveness of interventions to
prevent and control diabetes mellitus: a system-
atic review. Diabetes Care 2010;33:1872–1894
4. Grant RW, Kirkman MS. Trends in the evi-
dence level for the American Diabetes Associa-
tion’s “Standards of Medical Care in Diabetes”
from 2005 to 2014. Diabetes Care 2015;38:6–8
Diabetes Care Volume 38, Supplement 1, January 2015
Professional Practice Committee
Diabetes Care 2015;38(Suppl. 1):S3 | DOI: 10.2337/dc15-S002
The Professional Practice Committee
(PPC) of the American Diabetes Associa-
tion (ADA) is responsible for the “Stan-
dards of Medical Care in Diabetes”
position statement, referred to as the
“Standards of Care.” The PPC is a multidis-
ciplinary expert committee comprised of
physicians, diabetes educators, registered
dietitians, and others who have expertise
in a range of areas, including adult and
pediatric endocrinology, epidemiology,
public health, lipid research, hypertension,
and preconception and pregnancy care.
Appointment to the PPC is based on excel-
lence in clinical practice and/or research.
While the primary role of the PPC is to
review and update the Standards of
Care, it is also responsible for overseeing
the review and revisions of ADA’s position
statements and scientific statements.
All members of the PPC are required
to disclose potential conflicts of interest
with industry and/or other relevant or-
ganizations. These disclosures are dis-
cussed at the onset of each Standards
of Care revision meeting. Members of
the committee, their employer, and
their disclosed conflicts of interest are
listed in the “Professional Practice Com-
mittee for the Standards of Medical
Care in Diabetesd2015” table (see
p. S88).
For the current revision, PPC mem-
bers systematically searched MEDLINE
© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit,
and the work is not altered.
PROFESSIONAL PRACTICE COMMITTEE
S3
for human studies related to each sec- Edward W. Gregg, PhD; Silvio E. Inzucchi,
tion and published since 1 January 2014. MD; Mark E. Molitch, MD; John M.
Recommendations were revised based Morton, MD; Robert E. Ratner, MD;
on new evidence or, in some cases, to Linda M. Siminerio, RN, PhD, CDE; and
clarify the prior recommendation or Katherine R. Tuttle, MD.
match the strength of the wording to
the strength of the evidence. A table link- Members of the PPC
ing the changes in recommendations to
new evidence can be reviewed at http:// Richard W. Grant, MD, MPH (Chair)*
professional.diabetes.org/SOC. As for Thomas W. Donner, MD
all position statements, the Standards Judith E. Fradkin, MD
of Care position statement was reviewed
and approved by the Executive Committee Charlotte Hayes, MMSc, MS, RD, CDE,
of ADA’s Board of Directors, which in- ACSM CES
cludes health care professionals, scientists, William H. Herman, MD, MPH
and lay people. William C. Hsu, MD
Feedback from the larger clinical
Eileen Kim, MD
community was valuable for the 2015
revision of the Standards of Care. Read- Lori Laffel, MD, MPH
ers who wish to comment on the Stan- Rodica Pop-Busui, MD, PhD
dards of Medical Care in Diabetesd2015
Neda Rasouli, MD*
are invited to do so at http://professional
.diabetes.org/SOC. Desmond Schatz, MD
The ADA funds development of the Joseph A. Stankaitis, MD, MPH*
Standards of Care and all ADA position Tracey H. Taveira, PharmD, CDOE,
statements out of its general revenues CVDOE
and does not use industry support for
these purposes. Deborah J. Wexler, MD*
The PPC would like to thank the fol- *Subgroup leaders
lowing individuals who provided their ex-
pertise in reviewing and/or consulting with ADA Staff
the committee: Donald R. Coustan, MD;
Stephanie Dunbar, MPH, RD; Robert H. Jane L. Chiang, MD
Eckel, MD; Henry N. Ginsberg, MD; Erika Gebel Berg, PhD
 S4
SUMMARY OF REVISIONS
Standards of Medical Care in Diabetesd2015 :
Summary of Revisions
Diabetes Care 2015;38(Suppl. 1):S4 | DOI: 10.2337/dc15-S003
GENERAL CHANGES
Diabetes Care Supplement 1 was previ-
ously called Clinical Practice Recommen-
dations and included the “Standards of
Medical Care in Diabetes” and key
American Diabetes Association (ADA)
position statements. The supplement
has been renamed Standards of Medical
Care in Diabetes (“Standards”) and
contains a single ADA position state-
ment that provides evidence-based clin-
ical practice recommendations for
diabetes care.
Whereas the “Standards of Medical
Care in Diabetesd2015” should still
be viewed as a single document, it has
been divided into 14 sections, each in-
dividually referenced, to highlight im-
portant topic areas and to facilitate
navigation.
The supplement now includes an in-
dex to help readers find information on
particular topics.
SECTION CHANGES
Although the levels of evidence for sev-
eral recommendations have been up-
dated, these changes are not included
below as the clinical recommendations
have remained the same. Changes in ev-
idence level from, for example, C to E are
not noted below. The “Standards of
Medical Care in Diabetesd2015” con-
tains, in addition to many minor changes
that clarify recommendations or reflect
new evidence, the following more sub-
stantive revisions.
Section 2. Classification and
Diagnosis of Diabetes
The BMI cut point for screening over-
weight or obese Asian Americans for pre-
diabetes and type 2 diabetes was changed
to 23 kg/m2 (vs. 25 kg/m2) to reflect
the evidence that this population is at an
increased risk for diabetes at lower BMI
levels relative to the general population.
© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit,
and the work is not altered.
Diabetes Care Volume 38, Supplement 1, January 2015
Section 4. Foundations of Care:
Education, Nutrition, Physical Activity,
Smoking Cessation, Psychosocial Care,
and Immunization
The physical activity section was revised
to reflect evidence that all individuals,
including those with diabetes, should
be encouraged to limit the amount of
time they spend being sedentary by
breaking up extended amounts of time
(.90 min) spent sitting.
Due to the increasing use of e-cigarettes,
the Standards were updated to make clear
that e-cigarettes are not supported as an
alternative to smoking or to facilitate
smoking cessation.
Immunization recommendations were
revised to reflect recent Centers for Disease
Control and Prevention guidelines re-
garding PCV13 and PPSV23 vaccinations
in older adults.
Section 6. Glycemic Targets
The ADA now recommends a premeal
blood glucose target of 80–130 mg/dL,
rather than 70–130 mg/dL, to better re-
flect new data comparing actual average
glucose levels with A1C targets.
To provide additional guidance on the
successful implementation of continuous
glucose monitoring (CGM), the Standards
include new recommendations on assessing
a patient’s readiness for CGM and on
providing ongoing CGM support.
Section 7. Approaches to Glycemic
Treatment
The type 2 diabetes management algo-
rithm was updated to reflect all of the
currently available therapies for diabe-
tes management.
Section 8. Cardiovascular Disease and
Risk Management
The recommended goal for diastolic
blood pressure was changed from 80
mmHg to 90 mmHg for most people
with diabetes and hypertension to better
reflect evidence from randomized clinical
trials. Lower diastolic targets may still be
appropriate for certain individuals.
Recommendations for statin treat-
ment and lipid monitoring were revised
after consideration of 2013 American
College of Cardiology/American Heart
Association guidelines on the treatment
of blood cholesterol. Treatment initia-
tion (and initial statin dose) is now
driven primarily by risk status rather
than LDL cholesterol level.
With consideration for the new
statin treatment recommendations, the
Standards now provide the following
lipid monitoring guidance: a screening
lipid profile is reasonable at diabetes di-
agnosis, at an initial medical evaluation
and/or at age 40 years, and periodically
thereafter.
Section 9. Microvascular
Complications and Foot Care
To better target those at high risk for
foot complications, the Standards em-
phasize that all patients with insensate
feet, foot deformities, or a history of
foot ulcers have their feet examined at
every visit.
Section 11. Children and Adolescents
To reflect new evidence regarding the
risks and benefits of tight glycemic con-
trol in children and adolescents with di-
abetes, the Standards now recommend
a target A1C of ,7.5% for all pediatric
age-groups; however, individualization is
still encouraged.
Section 12. Management of Diabetes
in Pregnancy
This new section was added to the
Standards to provide recommendations
related to pregnancy and diabetes, in-
cluding recommendations regarding
preconception counseling, medications,
blood glucose targets, and monitoring.
Diabetes Care Volume 38, Supplement 1, January 2015 S5

American Diabetes Association

1. Strategies for Improving Care
Diabetes Care 2015;38(Suppl. 1):S5–S7 | DOI: 10.2337/dc15-S004

Recommendations
c A patient-centered communication style that incorporates patient prefer-
ences, assesses literacy and numeracy, and addresses cultural barriers to
care should be used. B
c Treatment decisions should be timely and founded on evidence-based guide-
lines that are tailored to individual patient preferences, prognoses, and
comorbidities. B
c Care should be aligned with components of the Chronic Care Model (CCM) to
ensure productive interactions between a prepared proactive practice team
and an informed activated patient. A

POSITION STATEMENT
c When feasible, care systems should support team-based care, community
involvement, patient registries, and decision support tools to meet patient
needs. B

DIABETES CARE CONCEPTS

In the following sections, different components of the clinical management of
patients with (or at risk for) diabetes are reviewed. We highlight the following three
themes that are woven throughout these sections that clinicians, policymakers, and
advocates should keep in mind:

1. Patient-Centeredness: Practice recommendations, whether based on evidence or

expert opinion, are intended to guide an overall approach to care. The science and art
of medicine come together when the clinician is faced with making treatment recom-
mendations for a patient who would not have met eligibility criteria for the studies on
which guidelines were based. Recognizing that one size does not fit all, these Standards
provide guidance for when and how to adapt recommendations (e.g., see Section 10.
Older Adults and Fig. 6.1. Approach to the Management of Hyperglycemia). Because
patients with diabetes are also at greatly increased risk of cardiovascular disease, a
patient-centered approach should include a comprehensive plan to reduce cardiovas-
cular risk by addressing blood pressure and lipid control, smoking cessation, weight
management, and healthy lifestyle changes that include adequate physical activity.
2. Diabetes Across the Life Span: An increasing proportion of patients with type 1
diabetes are adults. Conversely, and for less salutary reasons, the incidence of type
2 diabetes is increasing in children and young adults. Finally, patients both with type
1 diabetes and with type 2 diabetes are living well into older age, a stage of life for
which there is little evidence from clinical trials to guide therapy. All these de-
mographic changes highlight another challenge to high-quality diabetes care, which
is the need to improve coordination between clinical teams as patients pass through
different stages of the life span or the stages of pregnancy (preconception, preg-
nancy, and postpartum).
3. Advocacy for Patients With Diabetes: Advocacy can be defined as active support
and engagement to advance a cause or policy. Advocacy in the cause of improving the
lives of patients with (or at risk for) diabetes is an ongoing need. Given the tremendous Suggested citation: American Diabetes Associa-
toll that lifestyle factors such as obesity, physical inactivity, and smoking have on the tion. Strategies for improving care. Sec. 1. In
Standards of Medical Care in Diabetesd2015.
health of patients with diabetes, ongoing and energetic efforts are needed to address
Diabetes Care 2015;38(Suppl. 1):S5–S7
and change the societal determinants at the root of these problems. Within the more
© 2015 by the American Diabetes Association.
narrow domain of clinical practice guidelines, the application of evidence level grading Readers may use this article as long as the work
to practice recommendations can help identify areas that require more research is properly cited, the use is educational and not
investment (1). This topic is explored in more depth in Section 14. Diabetes Advocacy. for profit, and the work is not altered.
S6 Position Statement
CARE DELIVERY SYSTEMS
There has been steady improvement in the
proportion of diabetic patients achieving
recommended levels of A1C, blood pres-
sure, and LDL cholesterol in the last 10
years (2). The mean A1C nationally has
declined from 7.6% in 1999–2002 to
7.2% in 2007–2010 based on the National
Health and Nutrition Examination Survey
(NHANES) data (E.W. Gregg, Centers for
Disease Control and Prevention, personal
communication). This has been accompa-
nied by improvements in lipids and blood
pressure control and has led to substantial
reductions in end-stage microvascular
complications in patients with diabetes.
Nevertheless, between 33 and 49% of pa-
tients still do not meet targets for glyce-
mic, blood pressure, or cholesterol control,
and only 14% meet targets for all three
measures and nonsmoking status (2). Evi-
dence also suggests that progress in car-
diovascular risk factor control (particularly
tobacco use) may be slowing (2,3). Certain
patient groups, such as young adults and
patients with complex comorbidities, fi-
nancial or other social hardships, and/or
limited English proficiency, may present
particular challenges to goal-based care
(4–6). Persistent variation in quality of di-
abetes care across providers and across
practice settings even after adjusting for
patient factors indicates that there re-
mains potential for substantial system-
level improvements in diabetes care.
Chronic Care Model
Although numerous interventions to im-
prove adherence to the recommended
standards have been implemented, a ma-
jor barrier to optimal care is a delivery
system that too often is fragmented, lacks
clinical information capabilities, dupli-
cates services, and is poorly designed
for the coordinated delivery of chronic
care. The CCM has been shown to be an
effective framework for improving the
quality of diabetes care (7). The CCM in-
cludes six core elements for the provision
of optimal care of patients with chronic
disease: 1) delivery system design (mov-
ing from a reactive to a proactive care
delivery system where planned visits
are coordinated through a team-based
approach, 2) self-management support,
3) decision support (basing care on
evidence-based, effective care guide-
lines), 4) clinical information systems
(using registries that can provide patient-
specific and population-based support
Diabetes Care Volume 38, Supplement 1, January 2015
to the care team), 5) community resources
and policies (identifying or developing
resources to support healthy lifestyles),
and 6) health systems (to create a quality-
oriented culture). Redefining the roles
of the clinic staff and promoting self-
management on the part of the patient
are fundamental to the successful imple-
mentation of the CCM (8). Collaborative,
multidisciplinary teams are best suited to
provide care for people with chronic con-
ditions such as diabetes and to facilitate
patients’ self-management (9–12).
Key Objectives
The National Diabetes Education Pro-
gram (NDEP) maintains an online resource
(www.betterdiabetescare.nih.gov) to help
health care professionals design and im-
plement more effective health care de-
livery systems for those with diabetes.
Three specific objectives, with refer-
ences to literature that outlines practical
strategies to achieve each, are delin-
eated below.
Objective 1: Optimize Provider and Team
Behavior
The care team should prioritize timely and
appropriate intensification of lifestyle and/
or pharmaceutical therapy for patients who
have not achieved beneficial levels of blood
pressure, lipid, or glucose control (13).
Strategies such as explicit goal setting
with patients (14); identifying and address-
ing language, numeracy, or cultural barriers
to care (15–18); integrating evidence-based
guidelines and clinical information tools
into the process of care (19–21); and incor-
porating care management teams including
nurses, pharmacists, and other providers
(22–24) have each been shown to optimize
provider and team behavior and thereby
catalyze reductions in A1C, blood pressure,
and LDL cholesterol.
Objective 2: Support Patient Behavior
Change
Successful diabetes care requires a sys-
tematic approach to supporting patients’
behavior change efforts, including 1)
healthy lifestyle changes (physical activity,
healthy eating, tobacco cessation, weight
management, and effective coping), 2)
disease self-management (taking and
managing medication and, when clinically
appropriate, self-monitoring of glucose
and blood pressure), and 3) prevention
of diabetes complications (self-monitoring
of foot health; active participation in
screening for eye, foot, and renal compli-
cations; and immunizations). High-quality
diabetes self-management education
(DSME) has been shown to improve pa-
tient self-management, satisfaction, and
glucose control (25,26), as has delivery of
ongoing diabetes self-management sup-
port (DSMS), so that gains achieved during
DSME are sustained (27–29). National
DSME standards call for an integrated ap-
proach that includes clinical content and
skills, behavioral strategies (goal setting,
problem solving), and engagement with
emotional concerns in each needed curric-
ulum content area.
Objective 3: Change the Care System
An institutional priority in most successful
care systems is providing a high quality of
care (30). Changes that have been shown
to increase quality of diabetes care in-
clude basing care on evidence-based
guidelines (19); expanding the role of
teams and staff and implementing more
intensive disease management strategies
(6,22,31); redesigning the care process
(32); implementing electronic health re-
cord tools (33,34); activating and educat-
ing patients (35,36); removing financial
barriers and reducing patient out-of-
pocket costs for diabetes education, eye
exams, self-monitoring of blood glucose,
and necessary medications (6); and iden-
tifying/developing/engaging community
resources and public policy that support
healthy lifestyles (37). Recent initiatives
such as the Patient-Centered Medical
Home show promise for improving out-
comes through coordinated primary care
and offer new opportunities for team-
based chronic disease care (38). Addi-
tional strategies to improve diabetes
care include reimbursement structures
that, in contrast to visit-based billing, re-
ward the provision of appropriate and
high-quality care (39), and incentives
that accommodate personalized care
goals (6,40).
It is clear that optimal diabetes man-
agement requires an organized, system-
atic approach and the involvement of a
coordinated team of dedicated health
care professionals working in an envi-
ronment where patient-centered high-
quality care is a priority (6).
WHEN TREATMENT GOALS ARE
NOT MET
Some patients and their health care pro-
viders may not achieve the desired
treatment goals. Reassessing the treat-
ment regimen may require evaluation of
care.diabetesjournals.org
barriers such as income, health literacy,
diabetes-related distress, depression,
poverty, and competing demands, in-
cluding those related to family respon-
sibilities and dynamics. Other strategies
may include culturally appropriate and
enhanced DSME and DSMS, comanage-
ment with a diabetes team, referral to a
medical social worker for assistance
with insurance coverage, medication-
taking behavior assessment, or change
in pharmacological therapy. Initiation of
or increase in self-monitoring of blood
glucose, continuous glucose monitoring,
frequent patient contact, or referral to a
mental health professional or physician
with special expertise in diabetes may
be useful.
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1. Grant RW, Kirkman MS. Trends in the evi-
dence level for the American Diabetes Associ-
ation’s “Standards of Medical Care in
Diabetes” from 2005 to 2014. Diabetes Care
2015;38:6–8
2. Ali MK, Bullard KM, Saaddine JB, Cowie CC,
Imperatore G, Gregg EW. Achievement of goals
in U.S. diabetes care, 1999-2010. N Engl J Med
2013;368:1613–1624
3. Wang J, Geiss LS, Cheng YJ, et al. Long-term
and recent progress in blood pressure levels
among U.S. adults with diagnosed diabetes,
1988-2008. Diabetes Care 2011;34:1579–1581
4. Kerr EA, Heisler M, Krein SL, et al. Beyond
comorbidity counts: how do comorbidity type
and severity influence diabetes patients’ treat-
ment priorities and self-management? J Gen In-
tern Med 2007;22:1635–1640
5. Fernandez A, Schillinger D, Warton EM, et al.
Language barriers, physician-patient language
concordance, and glycemic control among in-
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of Northern California (DISTANCE). J Gen Intern
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6. TRIAD Study Group. Health systems, pa-
tients factors, and quality of care for diabetes:
a synthesis of findings from the TRIAD study.
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7. Stellefson M, Dipnarine K, Stopka C. The
chronic care model and diabetes management
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8. Coleman K, Austin BT, Brach C, Wagner EH.
Evidence on the Chronic Care Model in the new
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9. Piatt GA, Anderson RM, Brooks MM, et al. 3-
year follow-up of clinical and behavioral im-
provements following a multifaceted diabetes
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trolled trial. Diabetes Educ 2010;36:301–309
10. Renders CM, Valk GD, Griffin SJ, Wagner EH,
Eijk Van JT, Assendelft WJ. Interventions to im-
prove the management of diabetes in primary
care, outpatient, and community settings:
a systematic review. Diabetes Care 2001;24:
1821–1833
11. Katon WJ, Lin EHB, Von Korff M, et al. Col-
laborative care for patients with depression and
chronic illnesses. N Engl J Med 2010;363:2611–
2620
12. Parchman ML, Zeber JE, Romero RR, Pugh
JA. Risk of coronary artery disease in type 2 di-
abetes and the delivery of care consistent with
the chronic care model in primary care settings:
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13. Davidson MB. How our current medical
care system fails people with diabetes: lack of
timely, appropriate clinical decisions. Diabetes
Care 2009;32:370–372
14. Grant RW, Pabon-Nau L, Ross KM, Youatt EJ,
Pandiscio JC, Park ER. Diabetes oral medication
initiation and intensification: patient views
compared with current treatment guidelines.
Diabetes Educ 2011;37:78–84
15. Schillinger D, Piette J, Grumbach K, et al.
Closing the loop: physician communication
with diabetic patients who have low health lit-
eracy. Arch Intern Med 2003;163:83–90
16. Rosal MC, Ockene IS, Restrepo A, et al. Ran-
domized trial of a literacy-sensitive, culturally
tailored diabetes self-management interven-
tion for low-income Latinos: Latinos en Control.
Diabetes Care 2011;34:838–844
17. Osborn CY, Cavanaugh K, Wallston KA, et al.
Health literacy explains racial disparities in di-
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mun 2011;16(Suppl. 3):268–278
18. Rothman R, Malone R, Bryant B, Horlen C,
DeWalt D, Pignone M. The relationship between
literacy and glycemic control in a diabetes
disease-management program. Diabetes Educ
2004;30:263–273
19. O’Connor PJ, Bodkin NL, Fradkin J, et al. Di-
abetes performance measures: current status
and future directions. Diabetes Care 2011;34:
1651–1659
20. Garg AX, Adhikari NK, McDonald H, et al.
Effects of computerized clinical decision sup-
port systems on practitioner performance and
patient outcomes: a systematic review. JAMA
2005;293:1223–1238
21. Smith SA, Shah ND, Bryant SC, et al.; Evi-
dens Research Group. Chronic care model and
shared care in diabetes: randomized trial of an
electronic decision support system. Mayo Clin
Proc 2008;83:747–757
22. Jaffe MG, Lee GA, Young JD, Sidney S, Go
AS. Improved blood pressure control associated
with a large-scale hypertension program. JAMA
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23. Davidson MB, Ansari A, Karlan VJ. Effect of a
nurse-directed diabetes disease management
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and hospitalizations in a minority population.
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24. Stone RA, Rao RH, Sevick MA, et al. Active
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25. Duncan I, Birkmeyer C, Coughlin S, Li QE,
Sherr D, Boren S. Assessing the value of diabetes
education. Diabetes Educ 2009;35:752–760
Position Statement S7
26. Berikai P, Meyer PM, Kazlauskaite R, Savoy
B, Kozik K, Fogelfeld L. Gain in patients’ knowl-
edge of diabetes management targets is associ-
ated with better glycemic control. Diabetes
Care 2007;30:1587–1589
27. Funnell MM, Brown TL, Childs BP, et al. Na-
tional standards for diabetes self-management
education. Diabetes Care 2007;30:1630–1637
28. Klein S, Sheard NF, Pi-Sunyer X, et al.
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tion for the prevention and management of
type 2 diabetes: rationale and strategies: a state-
ment of the American Diabetes Association, the
North American Association for the Study of
Obesity, and the American Society for Clinical
Nutrition. Diabetes Care 2004;27:2067–2073
29. Norris SL, Zhang X, Avenell A, et al. Efficacy
of pharmacotherapy for weight loss in adults
with type 2 diabetes mellitus: a meta-analysis.
Arch Intern Med 2004;164:1395–1404
30. Tricco AC, Ivers NM, Grimshaw JM, et al.
Effectiveness of quality improvement strategies
on the management of diabetes: a systematic
review and meta-analysis. Lancet 2012;379:
2252–2261
31. Peikes D, Chen A, Schore J, Brown R. Effects
of care coordination on hospitalization, quality
of care, and health care expenditures among
Medicare beneficiaries: 15 randomized trials.
JAMA 2009;301:603–618
32. Feifer C, Nemeth L, Nietert PJ, et al. Differ-
ent paths to high-quality care: three archetypes
of top-performing practice sites. Ann Fam Med
2007;5:233–241
33. Reed M, Huang J, Graetz I, et al. Outpatient
electronic health records and the clinical care
and outcomes of patients with diabetes melli-
tus. Ann Intern Med 2012;157:482–489
34. Cebul RD, Love TE, Jain AK, Hebert CJ. Elec-
tronic health records and quality of diabetes
care. N Engl J Med 2011;365:825–833
35. Battersby M, Von Korff M, Schaefer J, et al.
Twelve evidence-based principles for implement-
ing self-management support in primary care. Jt
Comm J Qual Patient Saf 2010;36:561–570
36. Grant RW, Wald JS, Schnipper JL, et al.
Practice-linked online personal health records
for type 2 diabetes mellitus: a randomized con-
trolled trial. Arch Intern Med 2008;168:1776–
1782
37. Pullen-Smith B, Carter-Edwards L, Leathers
KH. Community health ambassadors: a mod-
el for engaging community leaders to pro-
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Public Health Manag Pract 2008;14(Suppl.):
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38. Bojadzievski T, Gabbay RA. Patient-centered
medical home and diabetes. Diabetes Care 2011;
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39. Rosenthal MB, Cutler DM, Feder J. The ACO
rulesdstriking the balance between participa-
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2011;365:e6
40. Washington AE, Lipstein SH. The Patient-
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 S8 Diabetes Care Volume 38, Supplement 1, January 2015

American Diabetes Association

2. Classification and Diagnosis of
Diabetes
Diabetes Care 2015;38(Suppl. 1):S8–S16 | DOI: 10.2337/dc15-S005

CLASSIFICATION
Diabetes can be classified into the following general categories:

1. Type 1 diabetes (due to b-cell destruction, usually leading to absolute insulin

deficiency)
2. Type 2 diabetes (due to a progressive insulin secretory defect on the background
of insulin resistance)
3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third
trimester of pregnancy that is not clearly overt diabetes)
POSITION STATEMENT

4. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes
(such as neonatal diabetes and maturity-onset diabetes of the young [MODY]), dis-
eases of the exocrine pancreas (such as cystic fibrosis), and drug- or chemical-induced
diabetes (such as in the treatment of HIV/AIDS or after organ transplantation)

This section reviews most common forms of diabetes but is not comprehensive.
For additional information, see the American Diabetes Association (ADA) position
statement “Diagnosis and Classification of Diabetes Mellitus” (1).
Assigning a type of diabetes to an individual often depends on the circumstances
present at the time of diagnosis, with individuals not necessarily fitting clearly into a
single category. For example, some patients cannot be clearly classified as having
type 1 or type 2 diabetes. Clinical presentation and disease progression may vary
considerably in both types of diabetes.
The traditional paradigms of type 2 diabetes occurring only in adults and type 1
diabetes only in children are no longer accurate, as both diseases occur in both cohorts.
Occasionally, patients with type 2 diabetes may present with diabetic ketoacidosis
(DKA). Children with type 1 diabetes typically present with the hallmark symptoms
of polyuria/polydipsia and occasionally with DKA. The onset of type 1 diabetes may be
variable in adults and may not present with the classic symptoms seen in children.
However, difficulties in diagnosis may occur in children, adolescents, and adults, with
the true diagnosis becoming more obvious over time.

DIAGNOSTIC TESTS FOR DIABETES

Diabetes may be diagnosed based on A1C criteria or plasma glucose criteria, either the
fasting plasma glucose (FPG) or the 2-h plasma glucose (2-h PG) value after a 75-g oral
glucose tolerance test (OGTT) (1,2) (Table 2.1).
The same tests are used to both screen for and diagnose diabetes. Diabetes may
be identified anywhere along the spectrum of clinical scenarios: in seemingly low-
risk individuals who happen to have glucose testing, in symptomatic patients, and in
higher-risk individuals whom the provider tests because of a suspicion of diabetes.
The same tests will also detect individuals with prediabetes.
A1C
The A1C test should be performed using a method that is certified by the NGSP and
standardized or traceable to the Diabetes Control and Complications Trial (DCCT) Suggested citation: American Diabetes Association.
reference assay. Although point-of-care (POC) A1C assays may be NGSP certified, Classification and diagnosis of diabetes. Sec. 2.
In Standards of Medical Care in Diabetesd2015.
proficiency testing is not mandated for performing the test, so use of POC assays for
Diabetes Care 2015;38(Suppl. 1):S8–S16
diagnostic purposes may be problematic and is not recommended.
© 2015 by the American Diabetes Association.
The A1C has several advantages to the FPG and OGTT, including greater conve- Readers may use this article as long as the work
nience (fasting not required), greater preanalytical stability, and less day-to-day is properly cited, the use is educational and not
perturbations during stress and illness. These advantages must be balanced by for profit, and the work is not altered.
care.diabetesjournals.org
Table 2.1—Criteria for the diagnosis
of diabetes
A1C $6.5%. The test should be performed
in a laboratory using a method that is
NGSP certified and standardized to the
DCCT assay.*
OR
FPG $126 mg/dL (7.0 mmol/L). Fasting is
defined as no caloric intake for at least
8 h.*
OR
2-h PG $200 mg/dL (11.1 mmol/L) during
an OGTT. The test should be performed
as described by the WHO, using
a glucose load containing the
equivalent of 75 g anhydrous glucose
dissolved in water.*
OR
In a patient with classic symptoms of
hyperglycemia or hyperglycemic crisis,
a random plasma glucose $200 mg/dL
(11.1 mmol/L).
*In the absence of unequivocal
hyperglycemia, results should be confirmed
by repeat testing.
greater cost, the limited availability of
A1C testing in certain regions of the
developing world, and the incomplete
correlation between A1C and average
glucose in certain individuals.
It is important to take age, race/
ethnicity, and anemia/hemoglobinopathies
into consideration when using the A1C to
diagnose diabetes.
Age
The epidemiological studies that formed
the framework for recommending A1C
to diagnose diabetes only included adult
populations. Therefore, it remains un-
clear if A1C and the same A1C cut point
should be used to diagnose diabetes in
children and adolescents (3–5).
Race/Ethnicity
A1C levels may vary with patients’ race/
ethnicity (6,7). For example, African
Americans may have higher A1C levels
than non-Hispanic whites despite simi-
lar fasting and postglucose load glucose
levels. A recent epidemiological study
found that, when matched for FPG,
African Americans (with and without di-
abetes) had higher A1C levels than non-
Hispanic whites, but also had higher levels
of fructosamine and glycated albumin
and lower levels of 1,5-anhydroglucitol,
suggesting that their glycemic burden
(particularly postprandially) may be
higher (8).
Hemoglobinopathies/Anemias
Interpreting A1C levels in the presence of
certain hemoglobinopathies and anemia
may be problematic. For patients with an
abnormal hemoglobin but normal red cell
turnover, such as those with the sickle cell
trait, an A1C assay without interference
from abnormal hemoglobins should be
used. An updated list of interferences is
available at www.ngsp.org/interf.asp. In
conditions associated with increased red
cell turnover, such as pregnancy (second
and third trimesters), recent blood loss
or transfusion, erythropoietin therapy,
or hemolysis, only blood glucose criteria
should be used to diagnose diabetes.
Fasting and 2-Hour Plasma Glucose
In addition to the A1C test, the FPG and
2-h PG may also be used to diagnose diabe-
tes (Table 2.1). The concordance between
the FPG and 2-h PG tests is imperfect, as
is the concordance between A1C and ei-
ther glucose-based test. National Health
and Nutrition Examination Survey
(NHANES) data indicate that an A1C cut
point of $6.5% identifies one-third
fewer cases of undiagnosed diabetes
than a fasting glucose cut point of
$126 mg/dL (7.0 mmol/L) (9). Numer-
ous studies have confirmed that, com-
pared with these A1C and FPG cut
points, the 2-h PG value diagnoses
more people with diabetes. Of note,
the lower sensitivity of A1C at the desig-
nated cut point may be offset by the
test’s ease of use and facilitation of
more widespread testing.
Unless there is a clear clinical diagno-
sis (e.g., a patient in a hyperglycemic
crisis or with classic symptoms of hyper-
glycemia and a random plasma glucose
$200 mg/dL), it is recommended that
the same test be repeated immediately
using a new blood sample for confirma-
tion because there will be a greater like-
lihood of concurrence. For example, if
the A1C is 7.0% and a repeat result is
6.8%, the diagnosis of diabetes is con-
firmed. If two different tests (such as
A1C and FPG) are both above the diagnos-
tic threshold, this also confirms the diag-
nosis. On the other hand, if a patient has
discordant results from two different
tests, then the test result that is above
the diagnostic cut point should be re-
peated. The diagnosis is made on the ba-
sis of the confirmed test. For example, if a
patient meets the diabetes criterion of
the A1C (two results $6.5%), but not
Position Statement S9
FPG (,126 mg/dL [7.0 mmol/L]), that
person should nevertheless be consid-
ered to have diabetes.
Since all the tests have preanalytic and
analytic variability, it is possible that an ab-
normal result (i.e., above the diagnostic
threshold), when repeated, will produce
a value below the diagnostic cut point.
This scenario is least likely for A1C, more
likely for FPG, and most likely for the 2-h
PG, especially if the glucose samples are
collected at room temperature and not
centrifuged promptly. Barring labora-
tory error, such patients will likely
have test results near the margins of
the diagnostic threshold. The health
care professional should follow the
patient closely and repeat the test in
3–6 months.
CATEGORIES OF INCREASED RISK
FOR DIABETES (PREDIABETES)
Recommendations
c Testing to assess risk for future di-
abetes in asymptomatic people
should be considered in adults of
any age who are overweight or
obese (BMI $25 kg/m 2 or $23
kg/m 2 in Asian Americans) and
who have one or more additional
risk factors for diabetes. For all
patients, particularly those who
are overweight or obese, testing
should begin at age 45 years. B
c If tests are normal, repeat testing
carried out at a minimum of 3-
year intervals is reasonable. C
c To test for prediabetes, the A1C,
FPG, and 2-h PG after 75-g OGTT
are appropriate. B
c In patients with prediabetes, iden-
tify and, if appropriate, treat other
cardiovascular disease (CVD) risk
factors. B
c Testing to detect prediabetes
should be considered in children
and adolescents who are over-
weight or obese and who have
two or more additional risk factors
for diabetes. E
Description
In 1997 and 2003, the Expert Commit-
tee on Diagnosis and Classification of
Diabetes Mellitus (10,11) recognized a
group of individuals whose glucose lev-
els did not meet the criteria for diabetes
but were too high to be considered
S10 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015

Table 2.2—Criteria for testing for diabetes or prediabetes in asymptomatic adults TYPE 1 DIABETES
1. Testing should be considered in all adults who are overweight (BMI $25 kg/m2 or $23 kg/m2 in
Asian Americans) and have additional risk factors: Recommendation
c physical inactivity c Inform the relatives of patients with
c first-degree relative with diabetes type 1 diabetes of the opportunity
c high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian to be tested for type 1 diabetes risk,
American, Pacific Islander) but only in the setting of a clinical
c women who delivered a baby weighing .9 lb or were diagnosed with GDM
research study. E
c hypertension ($140/90 mmHg or on therapy for hypertension)
c HDL cholesterol level ,35 mg/dL (0.90 mmol/L) and/or a triglyceride level .250 mg/dL
Immune-Mediated Diabetes
(2.82 mmol/L)
c women with polycystic ovary syndrome
This form, previously called “insulin-
c A1C $5.7%, IGT, or IFG on previous testing dependent diabetes” or “juvenile-onset
c other clinical conditions associated with insulin resistance (e.g., severe obesity, diabetes,” accounts for 5–10% of diabetes
acanthosis nigricans) and is due to cellular-mediated autoimmune
c history of CVD destruction of the pancreatic b-cells.
2. For all patients, particularly those who are overweight or obese, testing should Autoimmune markers include islet cell
begin at age 45 years. autoantibodies, autoantibodies to insu-
3. If results are normal, testing should be repeated at a minimum of 3-year intervals, with lin, autoantibodies to GAD (GAD65),
consideration of more frequent testing depending on initial results (e.g., those with
autoantibodies to the tyrosine phospha-
prediabetes should be tested yearly) and risk status.
tases IA-2 and IA-2b, and autoantibodies
to zinc transporter 8 (ZnT8). Type 1 di-
abetes is defined by the presence of one
normal. “Prediabetes” is the term used 9 to 25%). An A1C range of 6.0–6.5%
or more of these autoimmune markers.
for individuals with impaired fasting had a 5-year risk of developing diabe-
The disease has strong HLA associations,
glucose (IFG) and/or impaired glucose tes between 25–50% and a relative risk
with linkage to the DQA and DQB genes.
tolerance (IGT) and indicates an in- 20 times higher compared with an A1C
These HLA-DR/DQ alleles can be either
creased risk for the future develop- of 5.0% (12). In a community-based
predisposing or protective.
ment of diabetes. IFG and IGT should study of African American and non-
The rate of b-cell destruction is quite
not be viewed as clinical entities in Hispanic white adults without diabetes,
variable, being rapid in some individuals
their own right but rather risk factors baseline A1C was a stronger predictor
(mainly infants and children) and slow in
for diabetes (Table 2.2) and CVD. IFG of subsequent diabetes and cardiovas-
others (mainly adults). Children and
and IGT are associated with obesity cular events than fasting glucose (13).
adolescents may present with ketoaci-
(especially abdominal or visceral obe- Other analyses suggest that an A1C of
dosis as the first manifestation of the
sity), dyslipidemia with high triglycer- 5.7% is associated with a diabetes risk
disease. Others have modest fasting hy-
ides and/or low HDL cholesterol, and similar to that of the high-risk partici-
perglycemia that can rapidly change to
hypertension. pants in the Diabetes Prevention Pro-
severe hyperglycemia and/or ketoacido-
gram (DPP) (14).
sis with infection or other stress. Adults
Diagnosis Hence, it is reasonable to consider an
may retain sufficient b-cell function to
In 1997 and 2003, the Expert Commit- A1C range of 5.7–6.4% as identifying in-
prevent ketoacidosis for many years;
tee on Diagnosis and Classification of dividuals with prediabetes. As with those
such individuals eventually become de-
Diabetes Mellitus (10,11) defined IFG with IFG and/or IGT, individuals with an
pendent on insulin for survival and are
as FPG levels 100–125 mg/dL (5.6–6.9 A1C of 5.7–6.4% should be informed of
at risk for ketoacidosis. At this latter
mmol/L) and IGT as 2-h PG after 75-g their increased risk for diabetes and CVD
stage of the disease, there is little or
OGTT levels 140–199 mg/dL (7.8–11.0 and counseled about effective strategies
no insulin secretion, as manifested by
mmol/L). It should be noted that the to lower their risks (see Section 5. Preven-
low or undetectable levels of plasma
World Health Organization (WHO) and tion or Delay of Type 2 Diabetes). Similar
C-peptide. Immune-mediated diabetes
numerous diabetes organizations de- to glucose measurements, the continuum
fine the IFG cutoff at 110 mg/dL (6.1 of risk is curvilinear, so as A1C rises, the
mmol/L). diabetes risk rises disproportionately Table 2.3—Categories of increased risk
As with the glucose measures, sev- (12). Aggressive interventions and vigilant for diabetes (prediabetes)*
eral prospective studies that used A1C follow-up should be pursued for those FPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL
to predict the progression to diabetes considered at very high risk (e.g., those (6.9 mmol/L) (IFG)
demonstrated a strong, continuous with A1C .6.0%). OR
association between A1C and sub- Table 2.3 summarizes the categories 2-h PG in the 75-g OGTT 140 mg/dL (7.8
sequent diabetes. In a systematic re- of prediabetes. For recommendations mmol/L) to 199 mg/dL (11.0 mmol/L) (IGT)
view of 44,203 individuals from 16 regarding risk factors and screening for OR
cohort studies with a follow-up interval prediabetes, see p. S12 (“Testing for A1C 5.7–6.4%
averaging 5.6 years (range 2.8–12 Type 2 Diabetes and Prediabetes in *For all three tests, risk is continuous,
years), those with an A1C between Asymptomatic Adults” and “Testing for extending below the lower limit of the range
5.5–6.0% had a substantially increased Type 2 Diabetes and Prediabetes in Chil- and becoming disproportionately greater at
higher ends of the range.
risk of diabetes (5-year incidence from dren and Adolescents”).
care.diabetesjournals.org
commonly occurs in childhood and ado-
lescence, but it can occur at any age,
even in the 8th and 9th decades of life.
Autoimmune destruction of b-cells has
multiple genetic predispositions and is
also related to environmental factors
that are still poorly defined. Although pa-
tients are not typically obese when they
present with type 1 diabetes, obesity
should not preclude the diagnosis. These
patients are also prone to other autoim-
mune disorders such as Graves’ disease,
Hashimoto’s thyroiditis, Addison’s dis-
ease, vitiligo, celiac disease, autoimmune
hepatitis, myasthenia gravis, and perni-
cious anemia.
Idiopathic Diabetes
Some forms of type 1 diabetes have no
known etiologies. These patients have per-
manent insulinopenia and are prone to
ketoacidosis, but have no evidence of au-
toimmunity. Although only a minority of
patients with type 1 diabetes fall into this
category, of those who do, most are of
African or Asian ancestry. Individuals
with this form of diabetes suffer from ep-
isodic ketoacidosis and exhibit varying
degrees of insulin deficiency between epi-
sodes. This form of diabetes is strongly
inherited, lacks immunological evidence
for b-cell autoimmunity, and is not HLA
associated. An absolute requirement for
insulin replacement therapy in affected
patients may come and go.
Testing for Type 1 Diabetes
The incidence and prevalence of type 1
diabetes is increasing (15). Type 1 dia-
betic patients often present with acute
symptoms of diabetes and markedly ele-
vated blood glucose levels, and some are
diagnosed with life-threatening keto-
acidosis. Several studies suggest that mea-
suring islet autoantibodies in relatives of
those with type 1 diabetes may identify
individuals who are at risk for developing
type 1 diabetes. Such testing, coupled
with education about diabetes symptoms
and close follow-up in an observational
clinical study, may enable earlier identifi-
cation of type 1 diabetes onset. There is
evidence to suggest that early diagnosis
may limit acute complications (16) and
extend long-term endogenous insulin
production (17).
A recent study reported the risk of pro-
gression to type 1 diabetes from the time
of seroconversion to autoantibody posi-
tivity in three pediatric cohorts from Fin-
land, Germany, and the U.S. Of the 585
children who developed more than two
autoantibodies, nearly 70% developed
type 1 diabetes within 10 years and 84%
within 15 years (16,18). These findings are
highly significant because, while the Ger-
man group was recruited from offspring
of parents with type 1 diabetes, the Finn-
ish and American groups were recruited
from the general population. Remark-
ably, the findings in all three groups
were the same, suggesting that the
same sequence of events led to clinical
disease in both “sporadic” and genetic
cases of type 1 diabetes.
While there is currently a lack of
accepted screening programs, one
should consider referring relatives of
those with type 1 diabetes for antibody
testing for risk assessment in the
setting of a clinical research study
(http://www2.diabetestrialnet.org).
Widespread clinical testing of asymptom-
atic low-risk individuals is not currently
recommended due to lack of approved
therapeutic interventions. Higher-risk in-
dividuals may be tested, but only in the
context of a clinical research setting. In-
dividuals who test positive will be coun-
seled about the risk of developing
diabetes, diabetes symptoms, and DKA
prevention. Numerous clinical studies
are being conducted to test various meth-
ods of preventing type 1 diabetes in
those with evidence of autoimmunity
(www.clinicaltrials.gov).
TYPE 2 DIABETES
Recommendations
c Testing to detect type 2 diabetes
in asymptomatic people should
be considered in adults of any
age who are overweight or
obese (BMI $25 kg/m 2 or $23
kg/m 2 in Asian Americans) and
who have one or more addi-
tional risk factors for diabetes.
For all patients, particularly
those who are overweight or
obese, testing should begin at
age 45 years. B
c If tests are normal, repeat testing
carried out at a minimum of 3-year
intervals is reasonable. C
c To test for diabetes, the A1C, FPG,
and 2-h PG after 75-g OGTT are
appropriate. B
c In patients with diabetes, identify
and, if appropriate, treat other
CVD risk factors. B
Position Statement S11
c Testing to detect type 2 diabetes
should be considered in children
and adolescents who are over-
weight or obese and who have
two or more additional risk factors
for diabetes. E
Description
This form, previously referred to as “non-
insulin-dependent diabetes” or “adult-
onset diabetes,” accounts for ;90–95%
of all diabetes. Type 2 diabetes encom-
passes individuals who have insulin resis-
tance and usually relative (rather than
absolute) insulin deficiency. At least ini-
tially, and often throughout their lifetime,
these individuals may not need insulin
treatment to survive.
There are various causes of type 2 di-
abetes. Although the specific etiologies
are not known, autoimmune destruc-
tion of b-cells does not occur, and pa-
tients do not have any of the other
known causes of diabetes. Most, but
not all, patients with type 2 diabetes
are obese. Obesity itself causes some
degree of insulin resistance. Patients
who are not obese by traditional weight
criteria may have an increased percent-
age of body fat distributed predomi-
nantly in the abdominal region.
Ketoacidosis seldom occurs sponta-
neously in type 2 diabetes; when seen,
it usually arises in association with
the stress of another illness such as in-
fection. Type 2 diabetes frequently goes
undiagnosed for many years because hy-
perglycemia develops gradually and at
earlier stages is often not severe enough
for the patient to notice the classic di-
abetes symptoms. Nevertheless, such
patients are at an increased risk of
developing macrovascular and micro-
vascular complications.
Whereas patients with type 2 diabetes
may have insulin levels that appear nor-
mal or elevated, the higher blood glucose
levels in these patients would be expected
to result in even higher insulin values had
their b-cell function been normal. Thus,
insulin secretion is defective in these pa-
tients and insufficient to compensate for
insulin resistance. Insulin resistance may
improve with weight reduction and/or
pharmacological treatment of hyper-
glycemia but is seldom restored to normal.
The risk of developing type 2 diabetes
increases with age, obesity, and lack of
physical activity. It occurs more frequently
S12 Position Statement
in women with prior GDM, in those with
hypertension or dyslipidemia, and in cer-
tain racial/ethnic subgroups (African
American, American Indian, Hispanic/
Latino, and Asian American). It is often
associated with a strong genetic predis-
position, more so than type 1 diabetes.
However, the genetics of type 2 diabetes
is poorly understood.
Testing for Type 2 Diabetes and
Prediabetes in Asymptomatic Adults
Prediabetes and diabetes meet criteria for
conditions in which early detection is ap-
propriate. Both conditions are common
and impose significant clinical and public
health burdens. There is often a long pre-
symptomatic phase before the diagnosis
of type 2 diabetes. Simple tests to detect
preclinical disease are readily available.
The duration of glycemic burden is a strong
predictor of adverse outcomes. There are
effective interventions that prevent pro-
gression from prediabetes to diabetes
(see Section 5. Prevention or Delay of
Type 2 Diabetes) and reduce the risk
of diabetes complications (see Section
8. Cardiovascular Disease and Risk
Management and Section 9. Microvas-
cular Complications and Foot Care).
Approximately one-quarter of people
with diabetes in the U.S. are undiag-
nosed. Although screening of asymptom-
atic individuals to identify those with
prediabetes or diabetes might seem rea-
sonable, rigorous clinical trials to prove
the effectiveness of such screening have
not been conducted and are unlikely to
occur. A large European randomized con-
trolled trial compared the impact of
screening for diabetes and intensive
multifactorial intervention with that of
screening and routine care (19). General
practice patients between the ages of
40–69 years were screened for diabetes
and randomized by practice to intensive
treatment of multiple risk factors or rou-
tine diabetes care. After 5.3 years of
follow-up, CVD risk factors were modestly
but significantly improved with intensive
treatment compared with routine care,
but the incidence of first CVD events or
mortality was not significantly different
between the groups (19). The excellent
care provided to patients in the routine
care group and the lack of an unscreened
control arm limit our ability to prove
that screening and early intensive treat-
ment impact outcomes. Mathematical
modeling studies suggest that screening,
Diabetes Care Volume 38, Supplement 1, January 2015
beginning at age 30 or 45 years and
independent of risk factors, may be
cost-effective (,$11,000 per quality-
adjusted life-year gained) (20).
Additional considerations regarding
testing for type 2 diabetes and predia-
betes in asymptomatic patients include
the following:
Age
Testing recommendations for diabetes in
asymptomatic adults are listed in Table
2.2. Age is a major risk factor for diabetes.
Testing should begin at age 45 years for all
patients, particularly those who are over-
weight or obese.
BMI and Ethnicity
Testing should be considered in adults
of any age with BMI $25 kg/m2 and one
or more additional risk factors for dia-
betes. However, recent data (21) and
evidence from the ADA position state-
ment “BMI Cut Points to Identify At-Risk
Asian Americans for Type 2 Diabetes
Screening” (22) suggest that the BMI
cut point should be lower for the Asian
American population. For diabetes
screening purposes, the BMI cut points
fall consistently between 23–24 kg/m2
(sensitivity of 80%) for nearly all Asian
American subgroups (with levels slightly
lower for Japanese Americans). This
makes a rounded cut point of 23 kg/m2
practical. In determining a single BMI
cut point, it is important to balance sen-
sitivity and specificity so as to provide a
valuable screening tool without numer-
ous false positives. An argument can be
made to push the BMI cut point to lower
than 23 kg/m 2 in favor of increased
sensitivity; however, this would lead
to an unacceptably low specificity
(13.1%). Data from the WHO also sug-
gest that a BMI $23 kg/m2 should be
used to define increased risk in Asian
Americans (23).
Evidence also suggests that other
populations may benefit from lower
BMI cut points. For example, in a large
multiethnic cohort study, for an equiv-
alent incidence rate of diabetes, a BMI
of 30 kg/m2 in non-Hispanic whites was
equivalent to a BMI of 26 kg/m2 in Afri-
can Americans (24).
Medications
Certain medications, such as glucocorti-
coids, thiazide diuretics, and atypical anti-
psychotics (25), are known to increase the
risk of diabetes and should be considered
when ascertaining a diagnosis.
Diagnostic Tests
The A1C, FPG, and 2-h PG after 75-g OGTT
are appropriate for testing. It should be
noted that the tests do not necessarily
detect diabetes in the same individuals.
The efficacy of interventions for primary
prevention of type 2 diabetes (26–32) has
primarily been demonstrated among in-
dividuals with IGT, not for individuals with
isolated IFG or for those with prediabetes
defined by A1C criteria.
Testing Interval
The appropriate interval between tests is
not known (33). The rationale for the
3-year interval is that with this interval,
the number of false-positive tests that re-
quire confirmatory testing will be reduced
and individuals with false-negative tests
will be retested before substantial time
elapses and complications develop (33).
Community Screening
Ideally, testing should be carried out
within a health care setting because of
the need for follow-up and treatment.
Community testing outside a health care
setting is not recommended because peo-
ple with positive tests may not seek, or
have access to, appropriate follow-up test-
ing and care. Community testing may also
be poorly targeted; i.e., it may fail to reach
the groups most at risk and inappropri-
ately test those at very low risk or even
those who have already been diagnosed.
Testing for Type 2 Diabetes and
Prediabetes in Children and
Adolescents
In the last decade, the incidence and prev-
alence of type 2 diabetes in adolescents has
increased dramatically, especially in ethnic
populations (15). Recent studies question
the validity of A1C in the pediatric popula-
tion, especially among certain ethnicities,
and suggest OGTT or FPG as more suitable
diagnostic tests (34). However, many of
these studies do not recognize that diabe-
tes diagnostic criteria are based on long-
term health outcomes, and validations are
not currently available in the pediatric pop-
ulation (35). The ADA acknowledges the
limited data supporting A1C for diagnosing
diabetes in children and adolescents. How-
ever, aside from rare instances, such as cys-
tic fibrosis and hemoglobinopathies, the
ADA continues to recommend A1C in this
cohort (36,37). The modified recommenda-
tions of the ADA consensus report “Type 2
Diabetes in Children and Adolescents” are
summarized in Table 2.4.
care.diabetesjournals.org
Table 2.4—Testing for type 2 diabetes or
prediabetes in asymptomatic children*
Criteria
c Overweight (BMI .85th percentile
for age and sex, weight for height
.85th percentile, or weight .120%
of ideal for height)
Plus any two of the following risk factors:
c Family history of type 2 diabetes in
first- or second-degree relative
c Race/ethnicity (Native American,
African American, Latino, Asian
American, Pacific Islander)
c Signs of insulin resistance or
conditions associated with insulin
resistance (acanthosis nigricans,
hypertension, dyslipidemia,
polycystic ovary syndrome, or small-
for-gestational-age birth weight)
c Maternal history of diabetes or GDM
during the child’s gestation
Age of initiation: age 10 years or at onset
of puberty, if puberty occurs at a
younger age
Frequency: every 3 years
*Persons aged #18 years.
GESTATIONAL DIABETES MELLITUS
Recommendations
c Test for undiagnosed type 2 diabe-
tes at the first prenatal visit in
those with risk factors, using stan-
dard diagnostic criteria. B
c Test for GDM at 24–28 weeks of ges-
tation in pregnant women not pre-
viously known to have diabetes. A
c Screen women with GDM for per-
sistent diabetes at 6–12 weeks
postpartum, using the OGTT and
clinically appropriate nonpreg-
nancy diagnostic criteria. E
c Women with a history of GDM
should have lifelong screening for
the development of diabetes or
prediabetes at least every 3 years. B
c Women with a history of GDM
found to have prediabetes should
receive lifestyle interventions or
metformin to prevent diabetes. A
Definition
For many years, GDM was defined as
any degree of glucose intolerance that
was first recognized during pregnancy
(10), regardless of whether the condi-
tion may have predated the pregnancy
or persisted after the pregnancy. This
definition facilitated a uniform strategy
for detection and classification of GDM,
but it was limited by imprecision.
The ongoing epidemic of obesity and
diabetes has led to more type 2 diabetes
in women of childbearing age, resulting in
an increase in the number of pregnant
women with undiagnosed type 2 diabetes
(38). Because of the number of pregnant
women with undiagnosed type 2 diabe-
tes, it is reasonable to test women with
risk factors for type 2 diabetes (Table 2.2)
at their initial prenatal visit, using stan-
dard diagnostic criteria (Table 2.1).
Women with diabetes in the first trimes-
ter would be classified as having type 2
diabetes. GDM is diabetes diagnosed in
the second or third trimester of preg-
nancy that is not clearly overt diabetes.
Diagnosis
GDM carries risks for the mother and
neonate. Not all adverse outcomes are
of equal clinical importance. The Hyper-
glycemia and Adverse Pregnancy Out-
come (HAPO) study (39), a large-scale
(;25,000 pregnant women) multina-
tional cohort study, demonstrated that
risk of adverse maternal, fetal, and neo-
natal outcomes continuously increased
as a function of maternal glycemia at
24–28 weeks, even within ranges previ-
ously considered normal for pregnancy.
For most complications, there was no
threshold for risk. These results have
led to careful reconsideration of the di-
agnostic criteria for GDM. GDM diagno-
sis (Table 2.5) can be accomplished with
either of two strategies:
1. “One-step” 75-g OGTT or
2. “Two-step” approach with a 50-g
(nonfasting) screen followed by a
100-g OGTT for those who screen
positive
Different diagnostic criteria will identify
different degrees of maternal hypergly-
cemia and maternal/fetal risk, leading
some experts to debate, and disagree
on, optimal strategies for the diagnosis
of GDM.
One-Step Strategy
In the 2011 Standards of Care (40), the
ADA for the first time recommended
that all pregnant women not known to
have prior diabetes undergo a 75-g
OGTT at 24–28 weeks of gestation,
based on a recommendation of the In-
ternational Association of the Diabetes
and Pregnancy Study Groups (IADPSG)
(41). The IADPSG defined diagnostic cut
Position Statement S13
points for GDM as the average glucose
values (fasting, 1-h, and 2-h PG) in the
HAPO study at which odds for adverse
outcomes reached 1.75 times the esti-
mated odds of these outcomes at the
mean glucose levels of the study popu-
lation. This one-step strategy was an-
ticipated to significantly increase the
incidence of GDM (from 5–6% to ;15–
20%), primarily because only one abnormal
value, not two, became sufficient to make
the diagnosis. The ADA recognized that the
anticipated increase in the incidence of
GDM would have significant impact on
the costs, medical infrastructure capacity,
and potential for increased “medicaliza-
tion” of pregnancies previously catego-
rized as normal, but recommended these
diagnostic criteria changes in the context
of worrisome worldwide increases in obe-
sity and diabetes rates with the intent of
optimizing gestational outcomes for
women and their offspring.
The expected benefits to these preg-
nancies and offspring are inferred from
intervention trials that focused on
women with lower levels of hyperglyce-
mia than identified using older GDM di-
agnostic criteria and that found modest
benefits including reduced rates of large-
for-gestational-age births and preeclamp-
sia (42,43). It is important to note that
80–90% of women being treated for
mild GDM in two randomized controlled
trials (whose glucose values overlapped
with the thresholds recommended by
the IADPSG) could be managed with life-
style therapy alone. Data are lacking on
how the treatment of lower levels of hy-
perglycemia affects a mother’s risk for
the development of type 2 diabetes in
the future and her offspring’s risk for
obesity, diabetes, and other metabolic
dysfunction. Additional well-designed
clinical studies are needed to determine
the optimal intensity of monitoring and
treatment of women with GDM diag-
nosed by the one-step strategy.
Two-Step Strategy
In 2013, the National Institutes of Health
(NIH) convened a consensus develop-
ment conference on diagnosing GDM.
The 15-member panel had representatives
from obstetrics/gynecology, maternal-
fetal medicine, pediatrics, diabetes re-
search, biostatistics, and other related
fields to consider diagnostic criteria (44).
The panel recommended the two-step
approach of screening with a 1-h 50-g
S14 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015

Table 2.5—Screening for and diagnosis of GDM of diabetes are frequently characterized
One-step strategy by onset of hyperglycemia at an early age
Perform a 75-g OGTT, with plasma glucose measurement when patient is fasting and at 1 and (generally before age 25 years).
2 h, at 24–28 weeks of gestation in women not previously diagnosed with overt diabetes.
Neonatal Diabetes
The OGTT should be performed in the morning after an overnight fast of at least 8 h.
The diagnosis of GDM is made when any of the following plasma glucose values are met or
Diabetes diagnosed in the first 6 months of
exceeded: life has been shown not to be typical au-
c Fasting: 92 mg/dL (5.1 mmol/L) toimmune type 1 diabetes. This so-called
c 1 h: 180 mg/dL (10.0 mmol/L) neonatal diabetes can either be transient
c 2 h: 153 mg/dL (8.5 mmol/L) or permanent. The most common genetic
Two-step strategy defect causing transient disease is a defect
Step 1: Perform a 50-g GLT (nonfasting), with plasma glucose measurement at 1 h, at 24–28 on ZAC/HYAMI imprinting, whereas
weeks of gestation in women not previously diagnosed with overt diabetes. permanent neonatal diabetes is most
If the plasma glucose level measured 1 h after the load is $140 mg/dL* (7.8 mmol/L), proceed commonly a defect in the gene encoding
to a 100-g OGTT. the Kir6.2 subunit of the b-cell KATP chan-
Step 2: The 100-g OGTT should be performed when the patient is fasting. nel. Diagnosing the latter has implications,
The diagnosis of GDM is made if at least two of the following four plasma glucose levels since such children can be well managed
(measured fasting and 1 h, 2 h, 3 h after the OGTT) are met or exceeded: with sulfonylureas.
Carpenter/Coustan (56) or NDDG (57)

c Fasting 95 mg/dL (5.3 mmol/L)
c1h 180 mg/dL (10.0 mmol/L)
c2h 155 mg/dL (8.6 mmol/L)
c3h 140 mg/dL (7.8 mmol/L)
NDDG, National Diabetes Data Group.
*The ACOG recommends a lower threshold of 135 mg/dL (7.5 mmol/L) in high-risk ethnic
populations with higher prevalence of GDM; some experts also recommend 130 mg/dL
(7.2 mmol/L).
glucose load test (GLT) followed by a 3-h
100-g OGTT for those who screen
positive, a strategy commonly used in
the U.S.
Key factors reported in the NIH panel’s
decision-making process were the lack of
clinical trial interventions demonstrating
the benefits of the one-step strategy
and the potential negative consequences
of identifying a large new group of
women with GDM, including medicaliza-
tion of pregnancy with increased inter-
ventions and costs. Moreover, screening
with a 50-g GLT does not require fast-
ing and is therefore easier to accomplish
for many women. Treatment of higher
threshold maternal hyperglycemia, as
identified by the two-step approach, re-
duces rates of neonatal macrosomia,
large-for-gestational-age births, and
shoulder dystocia, without increasing
small-for-gestational-age births (45).
The American College of Obstetricians
and Gynecologists (ACOG) updated its
guidelines in 2013 and supported the
two-step approach (46).
Future Considerations
The conflicting recommendations from
expert groups underscore the fact that
there are data to support each strategy.
The decision of which strategy to
105 mg/dL (5.8 mmol/L)
190 mg/dL (10.6 mmol/L)
165 mg/dL (9.2 mmol/L)
145 mg/dL (8.0 mmol/L)
implement must therefore be made based
on the relative values placed on factors
that have yet to be measured (e.g., cost-
benefit estimation, willingness to change
practice based on correlation studies
rather than clinical intervention trial
results, relative role of cost consid-
erations, and available infrastructure lo-
cally, nationally, and internationally).
As the IADPSG criteria have been
adopted internationally, further evi-
dence has emerged to support im-
proved pregnancy outcomes with cost
savings (47) and may be the preferred
approach. In addition, pregnancies
complicated by GDM per IADPSG crite-
ria, but not recognized as such, have
comparable outcomes to pregnancies di-
agnosed as GDM by the more stringent
two-step criteria (48). There remains
strong consensus that establishing a uni-
form approach to diagnosing GDM will
benefit patients, caregivers, and policy-
makers. Longer-term outcome studies are
currently underway.
MONOGENIC DIABETES
SYNDROMES
Monogenic defects that cause b-cell dys-
function, such as neonatal diabetes and
MODY, represent a small fraction of pa-
tients with diabetes (,5%). These forms
Maturity-Onset Diabetes of the Young
MODY is characterized by impaired insulin
secretion with minimal or no defects in in-
sulin action. It is inherited in an autosomal
dominant pattern. Abnormalities at six ge-
netic loci on different chromosomes have
been identified to date. The most common
form is associated with mutations on chro-
mosome 12 in a hepatic transcription factor
referred to as hepatocyte nuclear factor
(HNF)-1a. A second form is associated
with mutations in the glucokinase gene
on chromosome 7p and results in a defec-
tive glucokinase molecule. Glucokinase
converts glucose to glucose-6-phosphate,
the metabolism of which, in turn, stimu-
lates insulin secretion by the b-cell. The
less common forms of MODY result from
mutations in other transcription factors, in-
cluding HNF-4a, HNF-1b, insulin promoter
factor (IPF)-1, and NeuroD1.
Diagnosis
Readily available commercial genetic
testing now enables a true genetic diag-
nosis. It is important to correctly diag-
nose one of the monogenic forms of
diabetes because these children may
be incorrectly diagnosed with type 1 or
type 2 diabetes, leading to suboptimal
treatment regimens and delays in diag-
nosing other family members (49).
The diagnosis of monogenic diabetes
should be considered in children with
the following findings:
○ Diabetes diagnosed within the first 6
months of life
○ Strong family history of diabetes but
without typical features of type 2 di-
abetes (nonobese, low-risk ethnic
group)
care.diabetesjournals.org
○ Mild fasting hyperglycemia (100–150
mg/dL [5.5–8.5 mmol/L]), especially if
young and nonobese
○ Diabetes with negative autoantibod-
ies and without signs of obesity or in-
sulin resistance
CYSTIC FIBROSIS–RELATED
DIABETES
Recommendations
c Annual screening for cystic fibrosis–
related diabetes (CFRD) with OGTT
should begin by age 10 years in all
patients with cystic fibrosis who
do not have CFRD. B A1C as a
screening test for CFRD is not rec-
ommended. B
c Patients with CFRD should be
treated with insulin to attain in-
dividualized glycemic goals. A
c In patients with cystic fibrosis and
IGT without confirmed diabetes,
prandial insulin therapy should be
considered to maintain weight. B
c Annual monitoring for complica-
tions of diabetes is recommended,
beginning 5 years after the diagno-
sis of CFRD. E
CFRD is the most common comorbidity
in people with cystic fibrosis, occurring in
about 20% of adolescents and 40–50% of
adults. Diabetes in this population is as-
sociated with worse nutritional status,
more severe inflammatory lung disease,
and greater mortality from respiratory
failure. Insulin insufficiency related to
partial fibrotic destruction of the islet
mass is the primary defect in CFRD. Ge-
netically determined function of the re-
maining b-cells and insulin resistance
associated with infection and inflamma-
tion may also play a role. While screening
for diabetes before the age of 10 years
can identify risk for progression to CFRD
in those with abnormal glucose tolerance,
there appears to be no benefit with re-
spect to weight, height, BMI, or lung func-
tion compared with those with normal
glucose tolerance ,10 years of age. The
use of continuous glucose monitoring
may be more sensitive than OGTT to de-
tect risk for progression to CFRD, but this
likely needs more evidence.
Encouraging data suggest that im-
proved screening (50,51) and aggressive
insulin therapy have narrowed the gap in
mortality between cystic fibrosis patients
with and without diabetes and have elim-
inated the sex difference in mortality (52).
Recent trials comparing insulin with oral
repaglinide showed no significant differ-
ence between the groups. However, an-
other study compared three different
groups: premeal insulin aspart, repagli-
nide, or oral placebo in cystic fibrosis pa-
tients with abnormal glucose tolerance.
Patients all had weight loss; however, in
the insulin-treated group, this pattern was
reversed, and they gained 0.39 (6 0.21)
BMI units (P 5 0.02). Patients in the
repaglinide-treated group had initial weight
gain, but this was not sustained by 6
months. The placebo group continued to
lose weight (53). Insulin remains the most
widely used therapy for CFRD (54).
Recommendations for the clinical man-
agement of CFRD can be found in the ADA
position statement “Clinical Care Guide-
lines for Cystic Fibrosis–Related Diabetes:
A Position Statement of the American
Diabetes Association and a Clinical Prac-
tice Guideline of the Cystic Fibrosis
Foundation, Endorsed by the Pediatric
Endocrine Society” (55).
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Diabetes Care Volume 38, Supplement 1, January 2015 S17

American Diabetes Association

3. Initial Evaluation and Diabetes
Management Planning
Diabetes Care 2015;38(Suppl. 1):S17–S19 | DOI: 10.2337/dc15-S006

MEDICAL EVALUATION

Recommendation
c Consider screening those with type 1 diabetes for autoimmune diseases (e.g.,
thyroid dysfunction, celiac disease) as appropriate. E

A complete medical evaluation should be performed at the initial visit to

1. Classify diabetes

POSITION STATEMENT
2. Detect diabetes complications
3. Review previous treatment and risk factor control in patients with established
diabetes
4. Assist in formulating a management plan
5. Provide a basis for continuing care

Laboratory tests appropriate to the evaluation of each patient’s medical condition

should be completed. A focus on the components of comprehensive care (Table 3.1)
will enable the health care team to optimally manage the patient with diabetes. Adults
who develop type 1 diabetes can develop additional autoimmune disorders, although
their risk is lower than that in children and adolescents with type 1 diabetes. For ad-
ditional details on autoimmune conditions, see Section 11. Children and Adolescents.

MANAGEMENT PLAN
People with diabetes should receive medical care from a collaborative, integrated team
with expertise in diabetes. This team may include physicians, nurse practitioners,
physician’s assistants, nurses, dietitians, pharmacists, and mental health professionals.
Individuals with diabetes must also assume an active role in their care.
The management plan should be written with input from the patient and family, the
physician, and other members of the health care team. Diabetes self-management
education (DSME) and ongoing diabetes support should be integral components of
the management plan. Various strategies and techniques should be used to enable
patients to self-manage diabetes, including providing education on problem-solving
skills for all aspects of diabetes management. Treatment goals and plans should be
individualized and take patient preferences into account. In developing the plan,
consideration should be given to the patient’s age, school/work schedule and con-
ditions, physical activity, eating patterns, social situation, cultural factors, presence
of diabetes complications, health priorities, and other medical conditions.

COMMON COMORBID CONDITIONS

Recommendation

c Consider assessing for and addressing common comorbid conditions Suggested citation: American Diabetes Associa-
(e.g., depression, obstructive sleep apnea) that may complicate diabetes tion. Initial evaluation and diabetes manage-
management. B ment planning. Sec. 3. In Standards of Medical
Care in Diabetesd2015. Diabetes Care 2015;38
(Suppl. 1):S17–S19
Improved disease prevention and treatment efficacy means that patients with
© 2015 by the American Diabetes Association.
diabetes are living longer, often with multiple comorbidities requiring complicated Readers may use this article as long as the work
medical regimens (1). Obesity, hypertension, and dyslipidemia are the most com- is properly cited, the use is educational and not
monly appreciated comorbidities. However, concurrent conditions, such as heart for profit, and the work is not altered.
S18 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015

Table 3.1—Components of the comprehensive diabetes evaluation

Fatty Liver Disease
Medical history Unexplained elevations of hepatic trans-
c Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding) aminase concentrations are signifi-
c Eating patterns, physical activity habits, nutritional status, and weight history; growth and cantly associated with higher BMI,
development in children and adolescents waist circumference, triglycerides, and
c Presence of common comorbidities, psychosocial problems, and dental disease fasting insulin and with lower HDL cho-
c Diabetes education history
lesterol. In a prospective analysis, diabe-
c Review of previous treatment regimens and response to therapy (A1C records)
c Current treatment of diabetes, including medications, medication adherence and barriers
tes was significantly associated with
thereto, meal plan, physical activity patterns, and readiness for behavior change incident nonalcoholic chronic liver dis-
c Results of glucose monitoring and patient’s use of data ease and with hepatocellular carcinoma
c DKA frequency, severity, and cause (10). Interventions that improve meta-
c Hypoglycemic episodes bolic abnormalities in patients with di-
c Hypoglycemia awareness abetes (weight loss, glycemic control,
c Any severe hypoglycemia: frequency and cause
and treatment with specific drugs for hy-
c History of diabetes-related complications
c Microvascular: retinopathy, nephropathy, neuropathy (sensory, including history of foot
perglycemia or dyslipidemia) are also
lesions; autonomic, including sexual dysfunction and gastroparesis) beneficial for fatty liver disease (11).
c Macrovascular: coronary heart disease, cerebrovascular disease, and peripheral arterial
disease Cancer
Physical examination Diabetes (possibly only type 2 diabetes)
c Height, weight, BMI is associated with increased risk of
c Blood pressure determination, including orthostatic measurements when indicated cancers of the liver, pancreas, endome-
c Fundoscopic examination
trium, colon/rectum, breast, and blad-
c Thyroid palpation
c Skin examination (for acanthosis nigricans and insulin injection sites)
der (12). The association may result
c Comprehensive foot examination from shared risk factors between type
c Inspection 2 diabetes and cancer (obesity, older
c Palpation of dorsalis pedis and posterior tibial pulses age, and physical inactivity), but may
c Presence/absence of patellar and Achilles reflexes also be due to hyperinsulinemia or
c Determination of proprioception, vibration, and monofilament sensation
hyperglycemia (13). Patients with diabe-
Laboratory evaluation tes should be encouraged to undergo
c A1C, if results not available within past 3 months
recommended age- and sex-appropriate
c If not performed/available within past year
c Fasting lipid profile, including total, LDL, and HDL cholesterol and triglycerides, as needed
cancer screenings and to reduce their
c Liver function tests modifiable cancer risk factors (obesity,
c Test for urine albumin excretion with spot urine albumin-to-creatinine ratio smoking, and physical inactivity).
c Serum creatinine and calculated glomerular filtration rate
c TSH in type 1 diabetes, dyslipidemia, or women over age 50 years
Fractures
Referrals Age-matched hip fracture risk is signifi-
c Eye care professional for annual dilated eye exam
cantly increased in both type 1 (sum-
c Family planning for women of reproductive age
c Registered dietitian for medical nutrition therapy
mary relative risk [RR] 6.3) and type 2
c DSME/DSMS diabetes (summary RR 1.7) in both sexes
c Dentist for comprehensive periodontal examination (14). Type 1 diabetes is associated with
c Mental health professional, if needed osteoporosis, but in type 2 diabetes an
DKA, diabetic ketoacidosis; DSMS, diabetes self-management support; TSH, thyroid-stimulating increased risk of hip fracture is seen de-
hormone. spite higher bone mineral density (BMD)
(15). In three large observational studies
of older adults, femoral neck BMD T
failure, depression, anxiety, and arthri- Obstructive Sleep Apnea score and the WHO Fracture Risk Algo-
tis, are found at higher rates in people Age-adjusted rates of obstructive sleep rithm (FRAX) score were associated with
with diabetes than in age-matched people apnea, a risk factor for cardiovascular hip and nonspine fracture, although
without diabetes and often complicate disease, are significantly higher (4- to fracture risk was higher in participants
diabetes management. These concurrent 10-fold) with obesity, especially with cen- with diabetes compared with those
conditions present clinical challenges tral obesity, in men and women (6). The without diabetes for a given T score and
related to polypharmacy, prevalent prevalence in general populations with age or for a given FRAX score (16). It is
symptoms, and complexity of care (2–5). type 2 diabetes may be up to 23% (7) appropriate to assess fracture history
and in obese participants enrolled in and risk factors in older patients with
Depression the Look AHEAD trial exceeded 80% diabetes and recommend BMD testing
As discussed in Section 4. Foundations (8). Treatment of sleep apnea signif- if appropriate for the patient’s age and sex.
of Care, depression, anxiety, and other icantly improves quality of life and Prevention strategies are the same as for
mental health symptoms are highly blood pressure control. The evidence the general population. For type 2 diabetic
prevalent in people with diabetes and for a treatment effect on glycemic control patients with fracture risk factors, avoid-
are associated with worse outcomes. is mixed (9). ing thiazolidinediones is warranted.
care.diabetesjournals.org
Cognitive Impairment
Diabetes is associated with a signifi-
cantly increased risk, and rate, of cogni-
tive decline and with increased risk of
dementia (17,18). In a 15-year prospec-
tive study of community-dwelling peo-
ple over the age of 60 years, the
presence of diabetes at baseline sig-
nificantly increased the age- and sex-
adjusted incidence of all-cause dementia,
Alzheimer disease, and vascular demen-
tia compared with rates in those with
normal glucose tolerance (19). In a sub-
study of the Action to Control Cardiovas-
cular Risk in Diabetes (ACCORD) clinical
trial, there were no differences in cogni-
tive outcomes between intensive and
standard glycemic control, although
there was significantly less of a decre-
ment in total brain volume, as measured
by MRI, in participants in the intensive
arm (20). The effects of hyperglycemia
and insulin on the brain are areas of in-
tense research interest.
Low Testosterone in Men
Mean levels of testosterone are lower in
men with diabetes compared with age-
matched men without diabetes, but
obesity is a major confounder (21).
Treatment in asymptomatic men is con-
troversial. The evidence that testoster-
one replacement affects outcomes is
mixed, and recent guidelines suggest
that testing and treating men without
symptoms are not recommended (22).
Periodontal Disease
Periodontal disease is more severe, but
not necessarily more prevalent, in patients
with diabetes than in those without (23).
Current evidence suggests that periodon-
tal disease adversely affects diabetes out-
comes, although evidence for treatment
benefits remains controversial (5).
Hearing Impairment
Hearing impairment, both in high fre-
quency and low/mid frequency ranges,
is more common in people with dia-
betes than in those without, perhaps
due to neuropathy and/or vascular
disease. In a National Health and Nutri-
tion Examination Survey (NHANES) anal-
ysis, hearing impairment was about
twice as prevalent in people with diabe-
tes compared with those without, after
adjusting for age and other risk factors
for hearing impairment (24).
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19. Ohara T, Doi Y, Ninomiya T, et al. Glucose
tolerance status and risk of dementia in the
community: the Hisayama study. Neurology
2011;77:1126–1134
20. Launer LJ, Miller ME, Williamson JD, et al.;
ACCORD MIND investigators. Effects of inten-
sive glucose lowering on brain structure
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(ACCORD MIND): a randomised open-label sub-
study. Lancet Neurol 2011;10:969–977
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Testosterone concentrations in diabetic and
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22. Bhasin S, Cunningham GR, Hayes FJ, et al.
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23. Khader YS, Dauod AS, El-Qaderi SS,
Alkafajei A, Batayha WQ. Periodontal status
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24. Bainbridge KE, Hoffman HJ, Cowie CC.
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 S20 Diabetes Care Volume 38, Supplement 1, January 2015

American Diabetes Association

4. Foundations of Care: Education,
Nutrition, Physical Activity,
Smoking Cessation, Psychosocial
Care, and Immunization
Diabetes Care 2015;38(Suppl. 1):S20–S30 | DOI: 10.2337/dc15-S007

DIABETES SELF-MANAGEMENT EDUCATION AND SUPPORT

Recommendations
c People with diabetes should receive diabetes self-management education
(DSME) and diabetes self-management support (DSMS) according to the na-
POSITION STATEMENT

tional standards for DSME and DSMS when their diabetes is diagnosed and as
needed thereafter. B
c Effective self-management and quality of life are the key outcomes of DSME
and DSMS and should be measured and monitored as part of care. C
c DSME and DSMS should address psychosocial issues, as emotional well-being
is associated with positive diabetes outcomes. C
c DSME and DSMS programs are appropriate venues for people with prediabe-
tes to receive education and support to develop and maintain behaviors that
can prevent or delay the onset of diabetes. C
c Because DSME and DSMS can result in cost-savings and improved outcomes B,
DSME and DSMS should be adequately reimbursed by third-party payers. E

DSME and DSMS are the ongoing processes of facilitating the knowledge, skill, and
ability necessary for diabetes self-care. This process incorporates the needs, goals,
and life experiences of the person with diabetes. The overall objectives of DSME and
DSMS are to support informed decision making, self-care behaviors, problem solv-
ing, and active collaboration with the health care team to improve clinical outcomes,
health status, and quality of life in a cost-effective manner (1).
DSME and DSMS are essential elements of diabetes care (2,3), and the current
national standards for DSME and DSMS (1) are based on evidence of their benefits.
Education helps people with diabetes initiate effective self-management and cope
with diabetes when they are first diagnosed. Ongoing DSME and DSMS also help
people with diabetes maintain effective self-management throughout a lifetime
of diabetes as they face new challenges and as treatment advances become avail-
able. DSME enables patients (including youth) to optimize metabolic control, pre-
vent and manage complications, and maximize quality of life in a cost-effective
manner (2,4).
Current best practice of DSME is a skill-based approach that focuses on helping
those with diabetes make informed self-management choices (1,2). DSME has
changed from a didactic approach focusing on providing information to empow-
erment models that focus on helping those with diabetes make informed self-
management decisions (2). Diabetes care has shifted to an approach that is more
patient centered and places the person with diabetes and his or her family at the Suggested citation: American Diabetes Associa-
tion. Foundations of care: education, nutrition,
center of the care model, working in collaboration with health care professionals.
physical activity, smoking cessation, psychoso-
Patient-centered care is respectful of and responsive to individual patient pref- cial care, and immunization. Sec. 4. In Standards
erences, needs, and values and ensures that patient values guide all decision of Medical Care in Diabetesd2015. Diabetes
making (5). Care 2015;38(Suppl. 1):S20–S30
© 2015 by the American Diabetes Association.
Evidence for the Benefits Readers may use this article as long as the work
Multiple studies have found that DSME is associated with improved diabetes knowl- is properly cited, the use is educational and not
edge, improved self-care behavior (1), improved clinical outcomes, such as lower for profit, and the work is not altered.
care.diabetesjournals.org
A1C (3,6–8), lower self-reported weight
(9,10), improved quality of life (8,11),
healthy coping (12,13), and lower costs
(14,15). Better outcomes were reported
for DSME interventions that were longer
and included follow-up support (DSMS)
(16–18), that were culturally (19,20) and
age appropriate (21,22), that were tai-
lored to individual needs and prefer-
ences, and that addressed psychosocial
issues and incorporated behavioral
strategies (2,12,23,24). Both individual
and group approaches have been found
effective (10,25). There is growing evi-
dence for the role of community health
workers (26), as well as peer (27–30) and
lay leaders (31), in delivering DSME and
DSMS (32).
Diabetes education is associated with
increased use of primary and preventive
services (14,33,34) and lower use of
acute, inpatient hospital services (14).
Patients who participate in diabetes ed-
ucation are more likely to follow best
practice treatment recommendations,
particularly among the Medicare popu-
lation, and have lower Medicare and in-
surance claim costs (15,33).
National Standards
The national standards for DSME and
DSMS are designed to define quality
and to assist diabetes educators in a va-
riety of settings to provide evidence-
based education and self-management
support (1). The standards are reviewed
and updated every 5 years by a task
force representing key organizations in-
volved in diabetes education and care.
Reimbursement
DSME, when provided by a program that
meets national standards for DSME and
is recognized by the American Diabetes
Association (ADA) or other approval
bodies, is reimbursed as part of the
Medicare program as overseen by the
Centers for Medicare & Medicaid Ser-
vices. DSME is also covered by most
health insurance plans. Although DSMS
has been shown to be instrumental
for improving outcomes and can be pro-
vided via phone calls and telehealth, it
currently has limited reimbursement as
in-person follow-up to DSME.
MEDICAL NUTRITION THERAPY
For many individuals with diabetes, the
most challenging part of the treatment
plan is determining what to eat. It is the
position of the ADA that there is not a
one-size-fits-all eating pattern for indi-
viduals with diabetes. The ADA also rec-
ognizes the integral role of nutrition
therapy in overall diabetes manage-
ment and recommends that each per-
son with diabetes be actively engaged
in self-management, education, and
treatment planning with his or her
health care provider, which includes
the collaborative development of an
individualized eating plan (35,36).
Therefore, it is important that all mem-
bers of the health care team be knowl-
edgeable about diabetes nutrition
therapy and support its implementa-
tion. See Table 4.1 for specific nutrition
recommendations.
Goals of Nutrition Therapy for Adults
With Diabetes
1. To promote and support healthful
eating patterns, emphasizing a variety
of nutrient-dense foods in appropriate
portion sizes, in order to improve
overall health and specifically to
○ Attain individualized glycemic,
blood pressure, and lipid goals
○ Achieve and maintain body weight
goals
○ Delay or prevent complications of
diabetes
2. To address individual nutrition needs
based on personal and cultural pref-
erences, health literacy and numer-
acy, access to healthful food choices,
willingness and ability to make be-
havioral changes, and barriers to
change.
3. To maintain the pleasure of eating by
providing positive messages about
food choices while limiting food
choices only when indicated by sci-
entific evidence.
4. To provide the individual with diabe-
tes with practical tools for day-to-day
meal planning rather than focusing
on individual macronutrients, micro-
nutrients, or single foods.
Nutrition therapy is an integral compo-
nent of diabetes prevention, manage-
ment, and self-management education.
All individuals with diabetes should re-
ceive individualized medical nutrition
therapy (MNT), preferably provided by a
registered dietitian who is knowledgeable
and skilled in providing diabetes MNT.
Comprehensive group diabetes education
Position Statement S21
programs including nutrition therapy or
individualized education sessions have re-
ported A1C decreases of 0.3–1% for type
1 diabetes (37–41) and 0.5–2% for type 2
diabetes (42–49).
Carbohydrate Management
Individuals with type 1 diabetes should
be offered intensive insulin therapy
education using the carbohydrate-
counting meal planning approach
(37,39,40,43,50), which has been shown
to improve glycemic control (50,51).
Consistent carbohydrate intake with re-
spect to time and amount can result in
improved glycemic control for individu-
als using fixed daily insulin doses (36). A
simple diabetes meal planning approach,
such as portion control or healthful food
choices, may be better suited for individ-
uals with health literacy and numeracy
concerns (36–40,42).
Weight Loss
Intensive lifestyle programs with fre-
quent follow-up are required to achieve
significant reductions in excess body
weight and improve clinical indicators
(52,53). Weight loss of 2–8 kg may pro-
vide clinical benefits in those with type 2
diabetes, especially early in the disease
process (52,53). Although several studies
resulted in improvements in A1C at 1 year
(52,54–56), not all weight-loss interven-
tions led to 1-year A1C improvements
(45,57–60). The most consistently identi-
fied changes in cardiovascular risk factors
were an increase in HDL cholesterol
(52,54,56,59,61), decrease in triglycerides
(52,61–63), and decrease in blood pres-
sure (52,54,57,59,61).
Weight-loss studies have used a vari-
ety of energy-restricted eating patterns,
with no clear evidence that one eating
pattern or optimal macronutrient dis-
tribution was ideal, suggesting that
macronutrient proportions should be
individualized (64). Studies show that
people with diabetes eat on average
about 45% of their calories from carbo-
hydrates, ;36–40% of calories from fat,
and ;16–18% from protein (57–59). A
variety of eating patterns have been
shown to be effective in managing di-
abetes, including Mediterranean-style
(53,65), Dietary Approaches to Stop
Hypertension (DASH)-style (66), and
plant-based (vegan or vegetarian) (67),
lower-fat (68), and lower-carbohydrate
patterns (68).
S22 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015

Table 4.1—Nutrition therapy recommendations

Topic Recommendations Evidence rating
Effectiveness of nutrition therapy c Nutrition therapy is recommended for all people with type 1 and type 2 A
diabetes as an effective component of the overall treatment plan.
c Individuals who have diabetes should receive individualized MNT to A
achieve treatment goals, preferably provided by a registered dietitian
familiar with the components of diabetes MNT.
c For individuals with type 1 diabetes, participation in an intensive, flexible A
insulin therapy education program using the carbohydrate-counting meal
planning approach can result in improved glycemic control.
c For individuals using fixed daily insulin doses, consistent carbohydrate B
intake with respect to time and amount can result in improved glycemic
control and reduce hypoglycemia risk.
c A simple diabetes meal planning approach, such as portion control or C
healthful food choices, may be better suited to individuals with type 2
diabetes with health and numeracy literacy concerns. This strategy also
may be effective for older adults.
c Because diabetes nutrition therapy can result in cost savings B and B, A, E
improved outcomes (e.g., A1C reduction) A, MNT should be adequately
reimbursed by insurance and other payers. E
Energy balance c For overweight or obese adults with type 2 diabetes or at risk for A
diabetes, reducing energy intake while maintaining a healthful eating
pattern is recommended to promote weight loss.
c Modest weight loss may provide clinical benefits in some individuals with A
diabetes, especially those early in the disease process. To achieve modest
weight loss, intensive lifestyle interventions with ongoing support are
recommended.
Eating patterns and macronutrient c Evidence suggests that there is not an ideal percentage of calories from B, E
distribution carbohydrate, protein, and fat for all people with diabetes B; therefore,
macronutrient distribution should be based on individualized assessment
of current eating patterns, preferences, and metabolic goals. E
c Carbohydrate amount and available insulin may be the most important A
factors influencing glycemic response after eating and should be
considered when developing the eating plan.
c Monitoring carbohydrate intake, whether by carbohydrate counting or B
experience-based estimation, remains critical in achieving glycemic
control.
c Carbohydrate intake from vegetables, fruits, whole grains, legumes, and B
dairy products should be advised over intake from other carbohydrate
sources, especially those that contain added fats, sugars, or sodium.
c Substituting low glycemic2load foods for higher glycemic2load foods C
may modestly improve glycemic control.
c Individuals at high risk for type 2 diabetes should be encouraged to B
achieve the U.S. Department of Agriculture recommendation for dietary
fiber (14 g fiber/1,000 kcal) and to consume foods containing whole
grains (one-half of grain intake).
c While substituting sucrose-containing foods for isocaloric amounts of A
other carbohydrates may have similar blood glucose effects,
consumption should be minimized to avoid displacing nutrient-dense
food choices.
c People with diabetes and those at risk should limit or avoid intake of B
sugar-sweetened beverages to reduce risk for weight gain and worsening
of cardiometabolic risk profile.
Protein c In individuals with type 2 diabetes, ingested protein appears to increase B
insulin response without increasing plasma glucose concentrations.
Therefore, carbohydrate sources high in protein should not be used to
treat or prevent hypoglycemia.
c Evidence is inconclusive regarding an ideal amount of total fat for people C, B
with diabetes; therefore, goals should be individualized. C Fat quality
appears to be far more important than quantity. B
c A Mediterranean-style eating pattern, rich in monounsaturated fatty B
acids, may benefit glycemic control and CVD risk factors and can
therefore be recommended as an effective alternative to a lower-fat,
higher-carbohydrate eating pattern.
Continued on p. S23
care.diabetesjournals.org Position Statement S23

Table 4.1—Continued
Topic Recommendations Evidence rating
Dietary fat c Increased consumption of foods containing long-chain omega-3 fatty acids B
(EPA and DHA), such as fatty fish, and omega-3 linolenic acid (ALA) is
recommended.
c The consumption of fish (particularly fatty fish) at least two times (two B
servings) per week is recommended.
c The amount of dietary saturated fat, cholesterol, and trans fat recommended C
for people with diabetes is the same as that recommended
for the general population.
c Evidence does not support recommending omega-3 supplements for people A
with diabetes for the prevention or treatment of cardiovascular events.
Micronutrients and herbal supplements c There is no clear evidence of benefit from vitamin or mineral C
supplementation in people with diabetes who do not have underlying
deficiencies.
c Routine supplementation with antioxidants, such as vitamins E and C and C
carotene, is not advised due to insufficient evidence of efficacy and
concerns related to long-term safety.
c There is insufficient evidence to support the routine use of C
micronutrients such as chromium, magnesium, and vitamin D to improve
glycemic control in people with diabetes.
c There is insufficient evidence to support the use of cinnamon or other E
herbs/supplements for the treatment of diabetes.
c It is recommended that individualized meal planning include optimization E
of food choices to meet recommended dietary allowance/dietary
reference intake for all micronutrients.
Alcohol c If adults with diabetes choose to drink alcohol, they should be advised to do so C
in moderation (no more than one drink per day for adult women and no
more than two drinks per day for adult men).
c Alcohol consumption may place people with diabetes at an increased risk for B
delayed hypoglycemia, especially if taking insulin or insulin secretagogues.
Education and awareness regarding the recognition and management
of delayed hypoglycemia are warranted.
Sodium c The recommendation for the general population to reduce sodium to less than B
2,300 mg/day is also appropriate for people with diabetes.
c For individuals with both diabetes and hypertension, further reduction in sodium B
intake should be individualized.

Macronutrients Proteins Protein’s effect on blood glucose levels in

Carbohydrates
Studies examining the ideal amount
of carbohydrate intake for people with
diabetes are inconclusive, although
monitoring carbohydrate intake and
considering the available insulin are
key strategies for improving postpran-
dial glucose control (37,69). The litera-
ture concerning glycemic index and
glycemic load in individuals with diabe-
tes is complex, although reductions in
A1C of 20.2% to 20.5% have been dem-
onstrated in some studies (64,70). A sys-
tematic review (64) found consumption
of whole grains was not associated with
improvements in glycemic control in
people with type 2 diabetes, although
it may reduce systemic inflammation.
One study did find a potential benefit of
whole-grain intake in reducing mortality
and cardiovascular disease (CVD) (71).
For people with diabetes and no evi-
dence of diabetic kidney disease, the
evidence is inconclusive about recom-
mending an ideal amount of protein
for optimizing glycemic control or for
improving one or more CVD risk mea-
sures (64). Therefore, these goals should
be individualized. For people with dia-
betes and diabetic kidney disease (with
albuminuria), reducing the amount of
dietary protein below usual intake is
not recommended because it does not
alter glycemic measures, cardiovascular
risk measures, or the course of glomer-
ular filtration rate decline (72,73). In in-
dividuals with type 2 diabetes, ingested
protein appears to increase insulin re-
sponse without increasing plasma glucose
concentrations (74). Therefore, carbohy-
drate sources high in protein should not
be used to treat or prevent hypoglycemia.
type 1 diabetes is less clear.
Fats
Limited research exists concerning the
ideal amount of fat for individuals with
diabetes. The Institute of Medicine has
defined an acceptable macronutrient
distribution range for all adults for total
fat of 20–35% of energy with no tolera-
ble upper intake level defined (75). The
type of fatty acids consumed is more
important than total amount of fat
when looking at metabolic goals and
risk of CVD (53,76,77). Multiple random-
ized controlled trials including patients
with type 2 diabetes have reported im-
proved glycemic control and/or blood lip-
ids when a Mediterranean-style eating
pattern, rich in monounsaturated fatty
acid, was consumed (53,57,78,79). A sys-
tematic review (64) concluded that
S24 Position Statement
supplementation with omega-3 fatty
acids did not improve glycemic control
but that higher dose supplementation
decreased triglycerides in individuals
with type 2 diabetes. Randomized con-
trolled trials also do not support recom-
mending omega-3 supplements for
primary or secondary prevention of CVD
(80–85). People with diabetes should be
advised to follow the guidelines for the
general population for the recommended
intakes of saturated fat, dietary choles-
terol, and trans fat (86).
Sodium
A review found that decreasing sodium
intake reduces blood pressure in those
with diabetes (87). Incrementally lower-
ing sodium intake (i.e., to 1,500 mg/day)
has shown beneficial effects on blood
pressure (87–89). The American Heart
Association recommends 1,500 mg/day
for African Americans, people diag-
nosed with hypertension, diabetes, or
chronic kidney disease, and those over
51 years of age (90). However, other
studies (88,89) have warranted caution
for universal sodium restriction to
1,500 mg in this population. For indi-
viduals with diabetes and hyperten-
sion, setting a sodium intake goal of
,2,300 mg/day should be considered
on an individual basis. Sodium intake
recommendations should take into ac-
count palatability, availability, additional
cost of specialty low-sodium products,
and the difficulty of achieving both low-
sodium recommendations and a nutri-
tionally adequate diet (86).
For complete discussion and refer-
ences of all recommendations, see the
ADA position statement “Nutrition Ther-
apy Recommendations for the Manage-
ment of Adults With Diabetes” (36).
PHYSICAL ACTIVITY
Recommendations
c Children with diabetes or predia-
betes should be encouraged to en-
gage in at least 60 min of physical
activity each day. B
c Adults with diabetes should be ad-
vised to perform at least 150 min/
week of moderate-intensity aero-
bic physical activity (50–70% of
maximum heart rate), spread
over at least 3 days/week with no
more than 2 consecutive days
without exercise. A
Diabetes Care Volume 38, Supplement 1, January 2015
c Evidence supports that all individ-
uals, including those with diabe-
tes, should be encouraged to
reduce sedentary time, particu-
larly by breaking up extended
amounts of time (.90 min) spent
sitting. B
c In the absence of contraindica-
tions, adults with type 2 diabetes
should be encouraged to perform
resistance training at least twice
per week. A
Exercise is an important part of the di-
abetes management plan. Regular exer-
cise has been shown to improve blood
glucose control, reduce cardiovascular
risk factors, contribute to weight loss,
and improve well-being. Furthermore,
regular exercise may prevent type 2 di-
abetes in high-risk individuals (91–93).
Structured exercise interventions of at
least 8 weeks’ duration have been
shown to lower A1C by an average of
0.66% in people with type 2 diabetes,
even with no significant change in BMI
(94). There are considerable data for the
health benefits (e.g., increased cardiovas-
cular fitness, muscle strength, improved
insulin sensitivity, etc.) of regular physical
activity for those with type 1 diabetes
(95). Higher levels of exercise intensity
are associated with greater improve-
ments in A1C and in fitness (96). Other
benefits include slowing the decline in
mobility among overweight patients
with diabetes (97). “Exercise and Type 2
Diabetes: The American College of Sports
Medicine and the American Diabetes As-
sociation: Joint Position Statement Exec-
utive Summary” reviews the evidence for
the benefits of exercise in people with
type 2 diabetes (98).
Exercise and Children
As is recommended for all children, chil-
dren with diabetes or prediabetes should
be encouraged to engage in at least 60
min of physical activity each day. Included
in the 60 min each day, children should
engage in vigorous-intensity aerobic
activity, muscle-strengthening activities,
and bone-strengthening activities at least
3 of those days (99).
Frequency and Type of Exercise
The U.S. Department of Health and
Human Services’ physical activity
guidelines for Americans (100) suggest
that adults over age 18 years do 150
min/week of moderate-intensity or 75
min/week of vigorous-intensity aerobic
physical activity, or an equivalent com-
bination of the two. In addition, the
guidelines suggest that adults also do
muscle-strengthening activities that in-
volve all major muscle groups 2 or more
days/week. The guidelines suggest that
adults over age 65 years, or those with
disabilities, follow the adult guidelines if
possible or, if this is not possible, be as
physically active as they are able.
Recent evidence supports that all in-
dividuals, including those with diabetes,
should be encouraged to reduce the
amount of time spent being sedentary
(e.g., working at a computer, watching
TV) particularly by breaking up ex-
tended amounts of time (.90 min)
spent sitting (101).
Exercise and Glycemic Control
Based on physical activity studies that in-
clude people with diabetes, it seems rea-
sonable to recommend that people with
diabetes follow the physical activity guide-
lines as for the general population. For
example, studies included in the meta-
analysis of effects of exercise interventions
on glycemic control (94) had a mean of 3.4
sessions/week, with a mean of 49 min/
session. Also, the Diabetes Prevention Pro-
gram (DPP) lifestyle intervention included
150 min/week of moderate-intensity exer-
cise and showed beneficial effect on gly-
cemia in those with prediabetes (91).
Clinical trials have provided strong evi-
dence for the A1C-lowering value of re-
sistance training in older adults with type
2 diabetes (98) and for an additive benefit
of combined aerobic and resistance exer-
cise in adults with type 2 diabetes
(102,103). If not contraindicated, patients
with type 2 diabetes should be encour-
aged to do at least two weekly sessions
of resistance exercise (exercise with free
weights or weight machines), with each
session consisting of at least one set of
five or more different resistance exercises
involving the large muscle groups (98).
Pre-exercise Evaluation
As discussed more fully in Section 8. Car-
diovascular Disease and Risk Manage-
ment, the best protocol for screening
asymptomatic diabetic patients for coro-
nary artery disease (CAD) remains unclear.
The ADA consensus report “Screening for
Coronary Artery Disease in Patients With
Diabetes” (104) on this issue concluded
that routine screening is not recommended.
Providers should use clinical judgment in
care.diabetesjournals.org
this area. Certainly, high-risk patients
should be encouraged to start with short
periods of low-intensity exercise and
slowly increase the intensity and dura-
tion. Providers should assess patients
for conditions that might contraindicate
certain types of exercise or predispose to
injury, such as uncontrolled hyperten-
sion, severe autonomic neuropathy, se-
vere peripheral neuropathy, a history of
foot lesions, and unstable proliferative
retinopathy. The patient’s age and pre-
vious physical activity level should be
considered. For type 1 diabetic patients,
the provider should customize the exer-
cise regimen to the individual’s needs.
Those with complications may require a
more thorough evaluation (95).
Exercise in the Presence of
Nonoptimal Glycemic Control
Hyperglycemia
When individuals with type 1 diabetes
are deprived of insulin for 12–48 h and
are ketotic, exercise can worsen hyper-
glycemia and ketosis (105); therefore,
vigorous activity should be avoided
with ketosis. However, it is not neces-
sary to postpone exercise based simply
on hyperglycemia, provided the patient
feels well and urine and/or blood ke-
tones are negative.
Hypoglycemia
In individuals taking insulin and/or insu-
lin secretagogues, physical activity can
cause hypoglycemia if medication dose
or carbohydrate consumption is not al-
tered. For individuals on these thera-
pies, added carbohydrate should be
ingested if pre-exercise glucose levels
are ,100 mg/dL (5.6 mmol/L). Hypogly-
cemia is less common in diabetic pa-
tients who are not treated with insulin
or insulin secretagogues, and no preven-
tive measures for hypoglycemia are usu-
ally advised in these cases.
Exercise in the Presence of Specific
Long-Term Complications of Diabetes
Retinopathy
If proliferative diabetic retinopathy or
severe nonproliferative diabetic reti-
nopathy is present, then vigorous aero-
bic or resistance exercise may be
contraindicated because of the risk of
triggering vitreous hemorrhage or reti-
nal detachment (106).
Peripheral Neuropathy
Decreased pain sensation and a higher
pain threshold in the extremities result
in an increased risk of skin breakdown
and infection and of Charcot joint de-
struction with some forms of exercise.
However, studies have shown that
moderate-intensity walking may not
lead to an increased risk of foot ulcers
or reulceration in those with peripheral
neuropathy (107). In addition, 150 min/
week of moderate exercise was re-
ported to improve outcomes in patients
with milder forms of neuropathy (106).
All individuals with peripheral neuropa-
thy should wear proper footwear and
examine their feet daily to detect le-
sions early. Anyone with a foot injury
or open sore should be restricted to
non–weight-bearing activities.
Autonomic Neuropathy
Autonomic neuropathy can increase the
risk of exercise-induced injury or ad-
verse event through decreased cardiac
responsiveness to exercise, postural hy-
potension, impaired thermoregulation,
impaired night vision due to impaired
papillary reaction, and higher suscepti-
bility to hypoglycemia (108). Cardiovas-
cular autonomic neuropathy is also an
independent risk factor for cardiovascu-
lar death and silent myocardial ischemia
(109). Therefore, individuals with dia-
betic autonomic neuropathy should
undergo cardiac investigation before
beginning physical activity more intense
than that to which they are accustomed.
Albuminuria and Nephropathy
Physical activity can acutely increase uri-
nary protein excretion. However, there
is no evidence that vigorous exercise
increases the rate of progression of
diabetic kidney disease, and there
appears to be no need for specific exer-
cise restrictions for people with diabetic
kidney disease (106).
SMOKING CESSATION
Recommendations
c Advise all patients not to smoke or
use tobacco products. A
c Include smoking cessation coun-
seling and other forms of treatment
as a routine component of diabetes
care. B
Results from epidemiological, case-
control, and cohort studies provide con-
vincing evidence to support the causal
link between cigarette smoking and
health risks. Much of the work document-
ing the effect of smoking on health does
Position Statement S25
not separately discuss results on subsets
of individuals with diabetes, but it does
suggest that the identified risks are at
least equivalent to those found in the
general population. Other studies of in-
dividuals with diabetes consistently
demonstrate that smokers (and people
exposed to secondhand smoke) have a
heightened risk of CVD, premature
death, and the microvascular complica-
tions of diabetes. Smoking may have a
role in the development of type 2 diabe-
tes (110). One study in smokers with
newly diagnosed type 2 diabetes found
that smoking cessation was associated
with amelioration of metabolic parame-
ters and reduced blood pressure and al-
buminuria at 1 year (111).
The routine and thorough assessment
of tobacco use is essential to prevent
smoking or encourage cessation. Nu-
merous large randomized clinical trials
have demonstrated the efficacy and
cost-effectiveness of brief counseling in
smoking cessation, including the use of
quit lines, in reducing tobacco use. For
the patient motivated to quit, the addi-
tion of pharmacological therapy to coun-
seling is more effective than either
treatment alone. Special considerations
should include assessment of level of
nicotine dependence, which is associ-
ated with difficulty in quitting and re-
lapse (112). Although some patients
may gain weight in the period shortly after
smoking cessation, recent research has
demonstrated that this weight gain does
not diminish the substantial CVD risk ben-
efit realized from smoking cessation (113).
There is no evidence that e-cigarettes
are a healthier alternative to smoking or
that e-cigarettes can facilitate smoking
cessation. Rigorous study of their short-
and long-term effects is needed in de-
termining their safety and efficacy and
their cardiopulmonary effects in com-
parison with smoking and standard ap-
proaches to smoking cessation (114).
PSYCHOSOCIAL ASSESSMENT AND
CARE
Recommendations
c Include assessment of the pa-
tient’s psychological and social
situation as an ongoing part
of the medical management of
diabetes. B
c Psychosocial screening and follow-
up may include, but are not limited
S26 Position Statement
to, attitudes about the illness,
expectations for medical man-
agement and outcomes, affect/
mood, general and diabetes-
related quality of life, resources
(financial, social, and emotional),
and psychiatric history. E
c Routinely screen for psychosocial
problems such as depression,
diabetes-related distress, anxi-
ety, eating disorders, and cogni-
tive impairment. B
c Older adults (aged $65 years)
with diabetes should be consid-
ered a high-priority population
for depression screening and
treatment. B
c Patients with comorbid diabetes
and depression should receive a
stepwise collaborative care ap-
proach for the management of
depression. A
Emotional well-being is an important part
of diabetes care and self-management.
Psychological and social problems can
impair the individual’s (115–117) or
family’s (118) ability to carry out
diabetes care tasks and therefore
compromise health status. There are
opportunities for the clinician to rou-
tinely assess psychosocial status in a
timely and efficient manner so that re-
ferral for appropriate services can be ac-
complished. A systematic review and
meta-analysis showed that psychosocial
interventions modestly but significantly
improved A1C (standardized mean dif-
ference 20.29%) and mental health out-
comes. However, there was a limited
association between the effects on A1C
and mental health, and no intervention
characteristics predicted benefit on both
outcomes (119).
Screening
Key opportunities for routine screening
of psychosocial status occur at diagno-
sis, during regularly scheduled manage-
ment visits, during hospitalizations, with
new-onset complications, or when prob-
lems with glucose control, quality of life,
or self-management are identified. Pa-
tients are likely to exhibit psychological
vulnerability at diagnosis, when their
medical status changes (e.g., end of the
honeymoon period), when the need for
intensified treatment is evident, and
when complications are discovered. De-
pression affects about 20–25% of people
Diabetes Care Volume 38, Supplement 1, January 2015
with diabetes (120) and increases the risk
for myocardial infarction and postmyo-
cardial infarction (121) and all-cause
mortality (122). There appears to be a
bidirectional relationship between de-
pression and both diabetes (123) and
metabolic syndrome (124).
Diabetes-related distress is distinct
from clinical depression and is very com-
mon (125–127) among people with di-
abetes and their family members (118).
Prevalence is reported as 18–45%, with
an incidence of 38–48% over 18 months.
High levels of distress are significantly
linked to A1C, self-efficacy, dietary and
exercise behaviors (13,126), and medi-
cation adherence (128). Other issues
known to impact self-management and
health outcomes include, but are not lim-
ited to, attitudes about the illness, ex-
pectations for medical management and
outcomes, anxiety, general and diabetes-
related quality of life, resources (finan-
cial, social, and emotional) (129), and
psychiatric history (130). Screening tools
are available for a number of these areas
(23,131,132).
Referral to Mental Health Specialist
Indications for referral to a mental
health specialist familiar with diabetes
management may include gross disre-
gard for the medical regimen (by self
or others) (133), depression, overall
stress related to work-life balance, pos-
sibility of self-harm, debilitating anxiety
(alone or with depression), indications
of an eating disorder (134), or cognitive
functioning that significantly impairs
judgment. It is preferable to incorporate
psychological assessment and treatment
into routine care rather than waiting for a
specific problem or deterioration in met-
abolic or psychological status (23,125). In
the Second Diabetes Attitudes, Wishes
and Needs (DAWN2) study, significant
diabetes-related distress was reported
by 44.6% of the participants, but only
23.7% reported that their health care
team asked them how diabetes impacted
their life (125).
Although the clinician may not feel
qualified to treat psychological prob-
lems (135), optimizing the patient-
provider relationship as a foundation
can increase the likelihood that the pa-
tient will accept referral for other ser-
vices. Collaborative care interventions
and use of a team approach have dem-
onstrated efficacy in diabetes and
depression (136,137). Interventions to
enhance self-management and address
severe distress have demonstrated effi-
cacy in diabetes-related distress (13).
IMMUNIZATION
Recommendations
c Provide routine vaccinations for
children and adults with diabetes
as for the general population. C
c Annually provide an influenza vac-
cine to all patients with diabetes
$6 months of age. C
c Administer pneumococcal poly-
saccharide vaccine 23 (PPSV23)
to all patients with diabetes $2
years of age. C
c Adults $65 years of age, if not
previously vaccinated, should re-
ceive pneumococcal conjugate
vaccine 13 (PCV13), followed by
PPSV23 6–12 months after initial
vaccination. C
c Adults $65 years of age, if previ-
ously vaccinated with PPSV23,
should receive a follow-up $12
months with PCV13. C
c Administer hepatitis B vaccination
to unvaccinated adults with diabe-
tes who are aged 19–59 years. C
c Consider administering hepatitis B
vaccination to unvaccinated adults
with diabetes who are aged $60
years. C
As for the general population, all chil-
dren and adults with diabetes should re-
ceive routine vaccinations (138,139).
Influenza and pneumonia are common,
preventable infectious diseases associ-
ated with high mortality and morbidity
in vulnerable populations, such as the
young and the elderly, and in people
with chronic diseases. Although there
are limited studies reporting the mor-
bidity and mortality of influenza and
pneumococcal pneumonia specifically
in people with diabetes, observational
studies of patients with a variety of
chronic illnesses, including diabetes,
show that these conditions are associ-
ated with an increase in hospitalizations
for influenza and its complications. Peo-
ple with diabetes may be at an increased
risk of the bacteremic form of pneumo-
coccal infection and have been reported
to have a high risk of nosocomial bacter-
emia, with a mortality rate as high as
50% (140). In a case-control series,
care.diabetesjournals.org
influenza vaccine was shown to reduce
diabetes-related hospital admission by
as much as 79% during flu epidemics
(141). There is sufficient evidence to
support that people with diabetes
have appropriate serologic and clinical
responses to these vaccinations. The
Centers for Disease Control and Preven-
tion (CDC) Advisory Committee on
Immunization Practices recommends in-
fluenza and pneumococcal vaccines for
all individuals with diabetes (http://
www.cdc.gov/vaccines/recs).
Pneumococcal Vaccines in Older
Adults
The ADA endorses a recent CDC advisory
panel that recommends that both
PCV13 and PPSV23 should be adminis-
tered routinely in series to all adults 65
years of age or older (142).
Pneumococcal Vaccine-Naïve People
Adults 65 years of age or older who have
not previously received pneumococcal
vaccine or whose previous vaccination
history is unknown should receive a
dose of PCV13 first, followed by PPSV23.
A dose of PPSV23 should be given 6–12
months following a dose of PCV13. If
PPSV23 cannot be given within this time
period, a dose of PPSV23 should be given
during the next visit. The two vaccines
should not be coadministered, and the
minimum interval between vaccine dos-
ing should be 8 weeks.
Previous Vaccination With PPSV23
Adults 65 years of age or older who pre-
viously have received one or more doses
of PPSV23 should also receive PCV13 if
they have not yet received it. PCV13
should be given no sooner than 12 months
after receipt of the most recent PPSV23
dose. For those for whom an additional
dose of PPSV23 is indicated, this subse-
quent PPSV23 dose should be given 6–12
months after PCV13 and at least 5 years
since the most recent dose of PPSV23.
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Beekman ATF, de Jonge P. Supplementation
with eicosapentaenoic omega-3 fatty acid
does not influence serum brain-derived
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tients with major depression: a randomized
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83. Holman RR, Paul S, Farmer A, Tucker L,
Stratton IM, Neil HA; Atorvastatin in Factorial
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84. Kromhout D, Geleijnse JM, de Goede J, et al.
n-3 fatty acids, ventricular arrhythmia-related
events, and fatal myocardial infarction in post-
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85. Bosch J, Gerstein HC, Dagenais GR, et al.;
ORIGIN Trial Investigators. n-3 fatty acids and
cardiovascular outcomes in patients with dys-
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86. Maillot M, Drewnowski A. A conflict be-
tween nutritionally adequate diets and meeting
the 2010 dietary guidelines for sodium. Am J
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87. Bray GA, Vollmer WM, Sacks FM,
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88. Thomas MC, Moran J, Forsblom C, et al.;
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90. Whelton PK, Appel LJ, Sacco RL, et al.
Sodium, blood pressure, and cardiovascular
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91. Knowler WC, Barrett-Connor E, Fowler SE,
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abetes with lifestyle intervention or metformin.
N Engl J Med 2002;346:393–403
92. Tuomilehto J, Lindstr öm J, Eriksson JG,
et al.; Finnish Diabetes Prevention Study Group.
Prevention of type 2 diabetes mellitus by
changes in lifestyle among subjects with im-
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93. Pan X-R, Li G-W, Hu Y-H, et al. Effects of diet
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94. Boulé NG, Haddad E, Kenny GP, Wells GA,
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95. Colberg SR, Riddell MC. Physical activity:
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97. Rejeski WJ, Ip EH, Bertoni AG, et al.; Look
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99. Janssen I, Leblanc AG. Systematic review of
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103. Church TS, Blair SN, Cocreham S, et al. Ef-
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moglobin A1c levels in patients with type 2
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104. Bax JJ, Young LH, Frye RL, Bonow RO,
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105. Chu L, Hamilton J, Riddell MC. Clinical man-
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106. Colberg SR. Exercise and Diabetes: A Clini-
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107. Lemaster JW, Reiber GE, Smith DG,
Heagerty PJ, Wallace C. Daily weight-bearing
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foot ulcers. Med Sci Sports Exerc 2003;35:
1093–1099
108. Spallone V, Ziegler D, Freeman R, et al.;
Toronto Consensus Panel on Diabetic Neuropa-
thy. Cardiovascular autonomic neuropathy in
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and management. Diabetes Metab Res Rev
2011;27:6392653
109. Pop-Busui R, Evans GW, Gerstein HC,
et al.; Action to Control Cardiovascular Risk in
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nomic dysfunction on mortality risk in the Ac-
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(ACCORD) trial. Diabetes Care 2010;33:1578–
1584
110. Jankowich M, Choudhary G, Taveira TH,
Wu W-C. Age-, race-, and gender-specific prev-
alence of diabetes among smokers. Diabetes
Res Clin Pract 2011;93:e101–e105
111. Voulgari C, Katsilambros N, Tentolouris N.
Smoking cessation predicts amelioration of mi-
croalbuminuria in newly diagnosed type 2 dia-
betes mellitus: a 1-year prospective study.
Metabolism 2011;60:1456–1464
112. Ranney L, Melvin C, Lux L, McClain E, Lohr
KN. Systematic review: smoking cessation inter-
vention strategies for adults and adults in spe-
cial populations. Ann Intern Med 2006;145:
845–856
113. Clair C, Rigotti NA, Porneala B, et al. Asso-
ciation of smoking cessation and weight change
with cardiovascular disease among adults with
and without diabetes. JAMA 2013;309:1014–
1021
114. Palazzolo DL. Electronic cigarettes and
vaping: a new challenge in clinical medicine
and public health. A literature review. Front
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115. Anderson RJ, Grigsby AB, Freedland KE,
et al. Anxiety and poor glycemic control:
a meta-analytic review of the literature. Int J
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116. Delahanty LM, Grant RW, Wittenberg E,
et al. Association of diabetes-related emotional
distress with diabetes treatment in primary care
patients with type 2 diabetes. Diabet Med 2007;
24:48–54
117. Anderson RJ, Freedland KE, Clouse RE,
Lustman PJ. The prevalence of comorbid depres-
sion in adults with diabetes: a meta-analysis. Di-
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118. Kovacs Burns K, Nicolucci A, Holt RIG,
et al.; DAWN2 Study Group. Diabetes Attitudes,
Wishes and Needs second study (DAWN2Ô):
cross-national benchmarking indicators for fam-
ily members living with people with diabetes.
Diabet Med 2013;30:778–788
119. Harkness E, Macdonald W, Valderas J,
Coventry P, Gask L, Bower P. Identifying psycho-
social interventions that improve both physical
and mental health in patients with diabetes:
a systematic review and meta-analysis. Diabe-
tes Care 2010;33:926–930
120. Bot M, Pouwer F, Zuidersma M, van Melle
JP, de Jonge P. Association of coexisting diabe-
tes and depression with mortality after myocar-
dial infarction. Diabetes Care 2012;35:503–509
121. Scherrer JF, Garfield LD, Chrusciel T, et al.
Increased risk of myocardial infarction in de-
pressed patients with type 2 diabetes. Diabetes
Care 2011;34:1729–1734
122. Sullivan MD, O’Connor P, Feeney P, et al.
Depression predicts all-cause mortality: epide-
miological evaluation from the ACCORD HRQL
substudy. Diabetes Care 2012;35:1708–1715
123. Chen P-C, Chan Y-T, Chen H-F, Ko M-C, Li C-Y.
Population-based cohort analyses of the bidi-
rectional relationship between type 2 diabetes
and depression. Diabetes Care 2013;36:376–
382
124. Pan A, Keum N, Okereke OI, et al. Bidirec-
tional association between depression and met-
abolic syndrome: a systematic review and meta-
analysis of epidemiological studies. Diabetes
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125. Nicolucci A, Kovacs Burns K, Holt RIG,
et al.; DAWN2 Study Group. Diabetes Attitudes,
Wishes and Needs second study (DAWN2Ô):
cross-national benchmarking of diabetes-
related psychosocial outcomes for people with
diabetes. Diabet Med 2013;30:767–777
126. Fisher L, Hessler DM, Polonsky WH,
Mullan J. When is diabetes distress clinically
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meaningful? Establishing cut points for the Di-
abetes Distress Scale. Diabetes Care 2012;35:
259–264
127. Fisher L, Glasgow RE, Strycker LA. The re-
lationship between diabetes distress and clini-
cal depression with glycemic control among
patients with type 2 diabetes. Diabetes Care
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128. Aikens JE. Prospective associations be-
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2472–2478
129. Gary TL, Safford MM, Gerzoff RB, et al.
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adults with diabetes in managed care: the
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mortality among persons with and without di-
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133. Rubin RR, Peyrot M. Psychological issues
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134. Young-Hyman DL, Davis CL. Disordered
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135. Beverly EA, Hultgren BA, Brooks KM,
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difficulties: a qualitative study. Diabetes Care
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136. Ciechanowski P. Diapression: an inte-
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140. Smith SA, Poland GA. Use of influenza and
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141. Colquhoun AJ, Nicholson KG, Botha JL,
Raymond NT. Effectiveness of influenza vaccine
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Morb Mortal Wkly Rep 2014;63:822–825
Diabetes Care Volume 38, Supplement 1, January 2015 S31

American Diabetes Association

5. Prevention or Delay of Type 2
Diabetes
Diabetes Care 2015;38(Suppl. 1):S31–S32 | DOI: 10.2337/dc15-S008

Recommendations
c Patients with impaired glucose tolerance (IGT) A, impaired fasting glucose
(IFG) E, or an A1C 5.7–6.4% E should be referred to an intensive diet and
physical activity behavioral counseling program targeting loss of 7% of body
weight and increasing moderate-intensity physical activity (such as brisk walk-
ing) to at least 150 min/week.
c Follow-up counseling may be important for success. B
c Based on the cost-effectiveness of diabetes prevention, such programs should
be covered by third-party payers. B

POSITION STATEMENT
c Metformin therapy for prevention of type 2 diabetes may be considered in
those with IGT A, IFG E, or an A1C 5.7–6.4% E, especially for those with BMI
.35 kg/m2, aged ,60 years, and women with prior gestational diabetes
mellitus (GDM). A
c At least annual monitoring for the development of diabetes in those with
prediabetes is suggested. E
c Screening for and treatment of modifiable risk factors for cardiovascular dis-
ease is suggested. B
c Diabetes self-management education (DSME) and support (DSMS) programs
are appropriate venues for people with prediabetes to receive education
and support to develop and maintain behaviors that can prevent or delay
the onset of diabetes. C

LIFESTYLE MODIFICATIONS
Randomized controlled trials have shown that individuals at high risk for developing
type 2 diabetes (IFG, IGT, or both) can significantly decrease the rate of diabetes
onset with particular interventions (1–5). These include intensive lifestyle modifi-
cation programs that have been shown to be very effective (;58% reduction after 3
years). Follow-up of all three large studies of lifestyle intervention has shown sus-
tained reduction in the rate of conversion to type 2 diabetes: 43% reduction at 20
years in the Da Qing study (6), 43% reduction at 7 years in the Finnish Diabetes
Prevention Study (DPS) (7), and 34% reduction at 10 years in the U.S. Diabetes Pre-
vention Program Outcomes Study (DPPOS) (8). A cost-effectiveness model suggested
that lifestyle interventions in the Diabetes Prevention Program (DPP) are cost-effective
(9). Actual cost data from the DPP and DPPOS confirm that the lifestyle interventions
are highly cost-effective (10). Group delivery of the DPP intervention in community
settings has the potential to be significantly less expensive while still achieving similar
weight loss (11). The Centers for Disease Control and Prevention (CDC) helps coordinate
the National Diabetes Prevention Program, a resource designed to bring evidence-
based lifestyle change programs for preventing type 2 diabetes to communities
(http://www.cdc.gov/diabetes/prevention/index.htm).
Given the clinical trial results and the known risks of progression of prediabetes to
diabetes, people with an A1C 5.7–6.4%, IGT, or IFG should be counseled on lifestyle Suggested citation: American Diabetes Associa-
changes with goals similar to those of the DPP (7% weight loss and moderate- tion. Prevention or delay of type 2 diabetes. Sec.
intensity physical activity of at least 150 min/week). 5. In Standards of Medical Care in Diabetesd2015.
Diabetes Care 2015;38(Suppl. 1):S31–S32
PHARMACOLOGICAL INTERVENTIONS © 2015 by the American Diabetes Association.
Readers may use this article as long as the work
Pharmacological agents, such as metformin, a-glucosidase inhibitors, orlistat, and is properly cited, the use is educational and not
thiazolidinediones, have each been shown to decrease incident diabetes to various for profit, and the work is not altered.
S32 Position Statement
degrees. Metformin has the strongest
evidence base and demonstrated long-
term safety as pharmacological therapy
for diabetes prevention (12). For other
drugs, cost, side effects, and lack of a
persistent effect require consideration.
Metformin was less effective than
lifestyle modification in the DPP and
DPPOS but may be cost-saving over a
10-year period (10). It was as effective
as lifestyle modification in participants
with BMI $35 kg/m2 but not signifi-
cantly better than placebo in those
over 60 years of age (1). In the DPP, for
women with a history of GDM, metfor-
min and intensive lifestyle modification
led to an equivalent 50% reduction in
diabetes risk (13). Metformin may be
recommended for very high-risk individu-
als (e.g., with history of GDM, who are very
obese, and/or those with more severe or
progressive hyperglycemia).
People with prediabetes often have
other cardiovascular risk factors, such as
obesity, hypertension, and dyslipidemia,
and are at an increased risk for cardiovas-
cular disease events. While treatment
goals are the same as for other patients
without diabetes, increased vigilance is
warranted to identify and treat these
and other risk factors (e.g., smoking).
DIABETES SELF-MANAGEMENT
EDUCATION AND SUPPORT
The standards for DSME and DSMS (see
Section 4. Foundations of Care) can also
apply to the education and support of
people with prediabetes. Currently, there
are significant barriers to the provision of
education and support to those with pre-
diabetes. However, the strategies for
Diabetes Care Volume 38, Supplement 1, January 2015
supporting successful behavior change
and the healthy behaviors recommended
for people with prediabetes are largely
identical to those for people with diabe-
tes. Given their training and experience,
providers of DSME and DSMS are partic-
ularly well equipped to assist people with
prediabetes in developing and maintain-
ing behaviors that can prevent or delay
the onset of diabetes (14–16).
References
1. Knowler WC, Barrett-Connor E, Fowler SE,
et al.; Diabetes Prevention Program Research
Group. Reduction in the incidence of type 2 di-
abetes with lifestyle intervention or metformin.
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2. Buchanan TA, Xiang AH, Peters RK, et al.
Preservation of pancreatic b-cell function and
prevention of type 2 diabetes by pharma-
cological treatment of insulin resistance in
high-risk hispanic women. Diabetes 2002;51:
2796–2803
3. Chiasson J-L, Josse RG, Gomis R, Hanefeld M,
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ised trial. Lancet 2002;359:2072–2077
4. Lin JS, O’Connor E, Evans CV, Senger CA,
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to promote a healthy lifestyle in persons with
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for the U.S. Preventive Services Task Force. Ann
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5. Paulweber B, Valensi P, Lindström J, et al. A
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6. Li G, Zhang P, Wang J, et al. The long-term
effect of lifestyle interventions to prevent dia-
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7. Lindström J, Ilanne-Parikka P, Peltonen M,
et al.; Finnish Diabetes Prevention Study Group.
Sustained reduction in the incidence of type 2
diabetes by lifestyle intervention: follow-up of
the Finnish Diabetes Prevention Study. Lancet
2006;368:1673–1679
8. Knowler WC, Fowler SE, Hamman RF, et al.;
Diabetes Prevention Program Research Group.
10-year follow-up of diabetes incidence and
weight loss in the Diabetes Prevention Program
Outcomes Study. Lancet 2009;374:1677–1686
9. Herman WH, Hoerger TJ, Brandle M, et al.;
Diabetes Prevention Program Research Group.
The cost-effectiveness of lifestyle modification
or metformin in preventing type 2 diabetes in
adults with impaired glucose tolerance. Ann In-
tern Med 2005;142:323–332
10. Diabetes Prevention Program Research
Group. The 10-year cost-effectiveness of life-
style intervention or metformin for diabetes
prevention: an intent-to-treat analysis of the
DPP/DPPOS. Diabetes Care 2012;35:723–730
11. Ackermann RT, Finch EA, Brizendine E, Zhou
H, Marrero DG. Translating the Diabetes Pre-
vention Program into the community. The
DEPLOY Pilot Study. Am J Prev Med 2008;35:
357–363
12. Diabetes Prevention Program Research
Group. Long-term safety, tolerability, and
weight loss associated with metformin in the
Diabetes Prevention Program Outcomes Study.
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13. Ratner RE, Christophi CA, Metzger BE, et al.;
Diabetes Prevention Program Research Group.
Prevention of diabetes in women with a history
of gestational diabetes: effects of metformin
and lifestyle interventions. J Clin Endocrinol
Metab 2008;93:4774–4779
14. Parekh D, Sarathi V, Shivane VK, Bandgar
TR, Menon PS, Shah NS. Pilot study to evaluate
the effect of short-term improvement in vita-
min D status on glucose tolerance in patients
with type 2 diabetes mellitus. Endocr Pract
2010;16:600–608
15. Shah M, Kaselitz E, Heisler M. The role of
community health workers in diabetes: update
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163–171
16. Heisler M. Overview of peer support mod-
els to improve diabetes self-management and
clinical outcomes. Diabetes Spectrum 2007;20:
214–221
Diabetes Care Volume 38, Supplement 1, January 2015 S33

American Diabetes Association

6. Glycemic Targets
Diabetes Care 2015;38(Suppl. 1):S33–S40 | DOI: 10.2337/dc15-S009

ASSESSMENT OF GLYCEMIC CONTROL

Two primary techniques are available for health providers and patients to assess the
effectiveness of the management plan on glycemic control: patient self-monitoring
of blood glucose (SMBG) or interstitial glucose and A1C. Continuous glucose mon-
itoring (CGM) may be a useful adjunct to SMBG in selected patients.

Recommendations

c When prescribed as part of a broader educational context, SMBG results may

help guide treatment decisions and/or self-management for patients using less
frequent insulin injections B or noninsulin therapies. E

POSITION STATEMENT
c When prescribing SMBG, ensure that patients receive ongoing instruction and
regular evaluation of SMBG technique, SMBG results, and their ability to use
SMBG data to adjust therapy. E
c Patients on multiple-dose insulin or insulin pump therapy should perform SMBG
prior to meals and snacks, occasionally postprandially, at bedtime, prior to ex-
ercise, when they suspect low blood glucose, after treating low blood glucose
until they are normoglycemic, and prior to critical tasks such as driving. B
c When used properly, CGM in conjunction with intensive insulin regimens is a useful
tool to lower A1C in selected adults (aged $25 years) with type 1 diabetes. A
c Although the evidence for A1C lowering is less strong in children, teens, and
younger adults, CGM may be helpful in these groups. Success correlates with
adherence to ongoing use of the device. B
c CGM may be a supplemental tool to SMBG in those with hypoglycemia un-
awareness and/or frequent hypoglycemic episodes. C
c Given variable adherence to CGM, assess individual readiness for continuing
use of CGM prior to prescribing. E
c When prescribing CGM, robust diabetes education, training, and support are
required for optimal CGM implementation and ongoing use. E

Self-monitoring of Blood Glucose

Major clinical trials of insulin-treated patients have included SMBG as part of the
multifactorial interventions to demonstrate the benefit of intensive glycemic con-
trol on diabetes complications. SMBG is thus an integral component of effective
therapy (1). SMBG allows patients to evaluate their individual response to therapy
and assess whether glycemic targets are being achieved. Integrating SMBG results
into diabetes management can be a useful tool for guiding medical nutrition therapy
and physical activity, preventing hypoglycemia, and adjusting medications (partic-
ularly prandial insulin doses). Evidence supports a correlation between greater
SMBG frequency and lower A1C (2). The patient’s specific needs and goals should
dictate SMBG frequency and timing.
Optimization
SMBG accuracy is dependent on the instrument and user (3), so it is important to
evaluate each patient’s monitoring technique, both initially and at regular intervals
thereafter. Optimal use of SMBG requires proper review and interpretation of the Suggested citation: American Diabetes Associa-
data, both by the patient and provider. Among patients who check their blood tion. Glycemic targets. Sec. 6. In Standards of
Medical Care in Diabetesd2015. Diabetes Care
glucose at least once daily, many report taking no action when results are high or 2015;38(Suppl. 1):S33–S40
low (4). In a yearlong study of insulin-naı̈ve patients with suboptimal initial glycemic
© 2015 by the American Diabetes Association.
control, a group trained in structured SMBG (a paper tool was used at least quarterly Readers may use this article as long as the work
to collect and interpret 7-point SMBG profiles taken on 3 consecutive days) reduced is properly cited, the use is educational and not
their A1C by 0.3 percentage points more than the control group (5). Patients should for profit, and the work is not altered.
S34 Position Statement
be taught how to use SMBG data to
adjust food intake, exercise, or phar-
macological therapy to achieve specific
goals. The ongoing need for and fre-
quency of SMBG should be reevaluated
at each routine visit. SMBG is especially
important for insulin-treated patients
to monitor for and prevent asymptom-
atic hypoglycemia and hyperglycemia.
For Patients on Intensive Insulin Regimens
Most patients on intensive insulin regi-
mens (multiple-dose insulin or insulin
pump therapy, including patients with
type 1 diabetes) should consider SMBG
prior to meals and snacks, occasionally
postprandially, at bedtime, prior to exer-
cise, when they suspect low blood glu-
cose, after treating low blood glucose
until they are normoglycemic, and prior
to critical tasks such as driving. For many
patients, this will require testing 6–10 (or
more) times daily, although individual
needs may vary. A database study of
almost 27,000 children and adolescents
with type 1 diabetes showed that, after
adjustment for multiple confounders, in-
creased daily frequency of SMBG was
significantly associated with lower A1C
(20.2% per additional test per day)
and with fewer acute complications (6).
For Patients Using Basal Insulin or
Oral Agents
The evidence is insufficient regarding
when to prescribe SMBG and how often
testing is needed for patients who do
not use an intensive insulin regimen,
such as those with type 2 diabetes using
basal insulin or oral agents.
Several randomized trials have called
into question the clinical utility and cost-
effectiveness of routine SMBG in noninsulin-
treated patients (7–9). A meta-analysis
suggested that SMBG reduced A1C by
0.25% at 6 months (10), but the reduction
subsides after 12 months (11). A key con-
sideration is that performing SMBG alone
does not lower blood glucose levels. To be
useful, the information must be integrated
into clinical and self-management plans.
Continuous Glucose Monitoring
Real-time CGM measures interstitial glu-
cose (which correlates well with plasma
glucose) and includes sophisticated
alarms for hypo- and hyperglycemic ex-
cursions, but the devices are still not
approved by the U.S. Food and Drug Ad-
ministration as a sole agent to monitor
glucose. CGMs require calibration with
Diabetes Care Volume 38, Supplement 1, January 2015
SMBG, with the latter still required for
making acute treatment decisions.
A 26-week randomized trial of 322
type 1 diabetic patients showed that
adults aged $25 years using intensive
insulin therapy and CGM experienced a
0.5% reduction in A1C (from ;7.6% to
7.1%), compared with those using inten-
sive insulin therapy with SMBG (12). Sen-
sor use in those aged ,25 years (children,
teens, and adults) did not result in signif-
icant A1C lowering, and there was no
significant difference in hypoglycemia
in any group. The greatest predictor of
A1C lowering for all age-groups was fre-
quency of sensor use, which was highest
in those aged $25 years and lower in
younger age-groups.
A recent registry study of 17,317 partic-
ipants confirmed that more frequent CGM
use is associated with lower A1C (13),
while another study showed that children
with .70% sensor use missed fewer
school days (14). Small randomized con-
trolled trials in adults and children with
baseline A1C 7.0–7.5% have confirmed fa-
vorable outcomes (A1C and hypoglycemia
occurrence) in groups using CGM, suggest-
ing that CGM may provide further benefit
for individuals with type 1 diabetes who
already have tight control (15,16).
A meta-analysis suggests that, com-
pared with SMBG, CGM is associ-
ated with short-term A1C lowering of
;0.26% (17). The long-term effective-
ness of CGM needs to be determined.
This technology may be particularly
useful in those with hypoglycemia
unawareness and/or frequent hypogly-
cemic episodes, although studies have
not shown significant reductions in se-
vere hypoglycemia (17,18). A CGM de-
vice equipped with an automatic low
glucose suspend feature has been ap-
proved by the U.S. Food and Drug Admin-
istration. The Automation to Simulate
Pancreatic Insulin Response (ASPIRE) trial
of 247 patients showed that sensor-
augmented insulin pump therapy with a
low glucose suspend significantly reduced
nocturnal hypoglycemia, without increas-
ing A1C levels for those over 16 years of
age (19). These devices may offer the op-
portunity to reduce severe hypoglycemia
for those with a history of nocturnal
hypoglycemia. Due to variable adher-
ence, optimal CGM use requires an as-
sessment of individual readiness for the
technology as well as initial and ongoing
education and support (13,20,21).
A1C Testing
Recommendations
c Perform the A1C test at least two
times a year in patients who are
meeting treatment goals (and who
have stable glycemic control). E
c Perform the A1C test quarterly in pa-
tients whose therapy has changed or
who are not meeting glycemic goals. E
c Use of point-of-care testing for
A1C provides the opportunity for
more timely treatment changes. E
A1C reflects average glycemia over sev-
eral months (3) and has strong predictive
value for diabetes complications (22,23).
Thus, A1C testing should be performed
routinely in all patients with diabetesdat
initial assessment and as part of continu-
ing care. Measurement approximately
every 3 months determines whether pa-
tients’ glycemic targets have been
reached and maintained. The frequency
of A1C testing should depend on the clin-
ical situation, the treatment regimen, and
the clinician’s judgment. Some patients
with stable glycemia well within target
may do well with testing only twice per
year. Unstable or highly intensively man-
aged patients (e.g., pregnant women with
type 1 diabetes) may require testing more
frequently than every 3 months (24).
A1C Limitations
The A1C test is subject to certain limita-
tions. Conditions that affect red blood cell
turnover (hemolysis, blood loss) and he-
moglobin variants must be considered,
particularly when the A1C result does
not correlate with the patient’s blood glu-
cose levels (3). For patients in whom A1C/
estimated average glucose (eAG) and
measured blood glucose appear discrep-
ant, clinicians should consider the possi-
bilities of hemoglobinopathy or altered
red blood cell turnover and the options
of more frequent and/or different timing
of SMBG or CGM use. Other measures of
chronic glycemia such as fructosamine
are available, but their linkage to average
glucose and their prognostic significance
are not as clear as for A1C.
The A1C does not provide a measure
of glycemic variability or hypoglycemia.
For patients prone to glycemic variabil-
ity, especially type 1 diabetic patients or
type 2 diabetic patients with severe in-
sulin deficiency, glycemic control is best
evaluated by the combination of results
care.diabetesjournals.org
from self-monitoring and the A1C. The
A1C may also confirm the accuracy of
the patient’s meter (or the patient’s re-
ported SMBG results) and the adequacy
of the SMBG testing schedule.
A1C and Mean Glucose
Table 6.1 shows the correlation between
A1C levels and mean glucose levels based
on two studies: the international A1C-
Derived Average Glucose (ADAG) trial,
which based the correlation with A1C
on frequent SMBG and CGM in 507 adults
(83% non-Hispanic whites) with type 1,
type 2, and no diabetes (25), and an em-
pirical study of the average blood glucose
levels at premeal, postmeal, and bedtime
associated with specified A1C levels using
data from the ADAG trial (21). The Amer-
ican Diabetes Association (ADA) and the
American Association for Clinical Chemis-
try have determined that the correlation
(r 5 0.92) in the ADAG trial is strong
enough to justify reporting both the A1C
result and the eAG result when a clinician
orders the A1C test. Clinicians should
note that the mean plasma glucose num-
bers in the table are based on ;2,800
readings per A1C in the ADAG trial.
A1C Differences in Ethnic Populations and
Children
In the ADAG study, there were no signif-
icant differences among racial and ethnic
groups in the regression lines between
A1C and mean glucose, although there
was a trend toward a difference between
the African/African American and non-
Hispanic white cohorts. A small study
Table 6.1—Mean glucose levels for specified A1C levels (21,25)
Mean plasma glucose*
Mean fasting glucose Mean premeal glucose
A1C (%) mg/dL mmol/L mg/dL
6 126 7.0
,6.5
6.5–6.99
7 154 8.6
7.0–7.49
7.5–7.99
8 183 10.2
8–8.5
9 212 11.8
10 240 13.4
11 269 14.9
12 298 16.5
A calculator for converting A1C results into eAG, in either mg/dL or mmol/L, is available at http://professional.diabetes.org/eAG.
*These estimates are based on ADAG data of ;2,700 glucose measurements over 3 months per A1C measurement in 507 adults with type 1, type 2,
and no diabetes. The correlation between A1C and average glucose was 0.92 (25).
Position Statement S35
comparing A1C to CGM data in children
hypoglycemia or other adverse ef-
with type 1 diabetes found a highly sta-
fects of treatment. Appropriate
tistically significant correlation between
patients might include those with
A1C and mean blood glucose, although
short duration of diabetes, type 2
the correlation (r 5 0.7) was significantly
diabetes treated with lifestyle or
lower than in the ADAG trial (26).
metformin only, long life expec-
Whether there are significant differences
tancy, or no significant cardiovas-
in how A1C relates to average glucose in
cular disease (CVD). C
children or in different ethnicities is an
c Less stringent A1C goals (such as
area for further study (27,28). For the
,8%) may be appropriate for pa-
time being, the question has not led to
tients with a history of severe hypo-
different recommendations about testing
glycemia, limited life expectancy,
A1C or to different interpretations of the
advanced microvascular or macro-
clinical meaning of given levels of A1C in
vascular complications, extensive co-
those populations.
morbid conditions, or long-standing
A1C GOALS diabetes in whom the general goal
For glycemic goals in children, please refer is difficult to attain despite diabetes
to Section 11. Children and Adolescents. For self-management education, ap-
glycemic goals in pregnant women, please propriate glucose monitoring,
refer to Section 12. Management of Diabe- and effective doses of multiple
tes in Pregnancy. glucose-lowering agents including
insulin. B
Recommendations
c Lowering A1C to approximately 7%
A1C and Microvascular Complications
or less has been shown to reduce
Hyperglycemia defines diabetes, and
microvascular complications of dia-
glycemic control is fundamental to
betes, and, if implemented soon af-
diabetes management. The Diabetes
ter the diagnosis of diabetes, it is
Control and Complications Trial (DCCT)
associated with long-term reduc-
(1), a prospective randomized controlled
tion in macrovascular disease.
trial of intensive versus standard glyce-
Therefore, a reasonable A1C goal
mic control in patients with relatively
for many nonpregnant adults is
recently diagnosed type 1 diabetes
,7%. B
showed definitively that improved glyce-
c Providers might reasonably sug-
mic control is associated with signifi-
gest more stringent A1C goals
cantly decreased rates of microvascular
(such as ,6.5%) for selected in-
(retinopathy and diabetic kidney dis-
dividual patients if this can
ease) and neuropathic complications.
be achieved without significant
Follow-up of the DCCT cohorts in the
Mean postmeal glucose Mean bedtime glucose
mg/dL mg/dL mg/dL
122 118 144 136
142 139 164 153
152 152 176 177
167 155 189 175
178 179 206 222
S36 Position Statement
Epidemiology of Diabetes Interventions
and Complications (EDIC) study (29,30)
demonstrated persistence of these
microvascular benefits in previously
intensively treated subjects, even
though their glycemic control approxi-
mated that of previous standard arm
subjects during follow-up.
The Kumamoto Study (31) and UK
Prospective Diabetes Study (UKPDS)
(32,33) confirmed that intensive
glycemic control was associated with sig-
nificantly decreased rates of microvascu-
lar and neuropathic complications in
type 2 diabetic patients. Long-term
follow-up of the UKPDS cohorts showed
enduring effects of early glycemic con-
trol on most microvascular complica-
tions (34).
Three landmark trials (Action to Con-
trol Cardiovascular Risk in Diabetes
[ACCORD], Action in Diabetes and Vas-
cular Disease: Preterax and Diamicron
MR Controlled Evaluation [ADVANCE],
and Veterans Affairs Diabetes Trial
[VADT]) showed that lower A1C levels
were associated with reduced onset or
progression of microvascular complica-
tions (35–37).
Epidemiological analyses of the DCCT
(1) and UKPDS (38) demonstrate a
curvilinear relationship between A1C
and microvascular complications.
Such analyses suggest that, on a popu-
lation level, the greatest number of
complications will be averted by taking
patients from very poor control to fair/
good control. These analyses also sug-
gest that further lowering of A1C from
7% to 6% is associated with further re-
duction in the risk of microvascular
complications, though the absolute
risk reductions become much smaller.
Given the substantially increased risk
of hypoglycemia in type 1 diabetes tri-
als and in recent type 2 diabetes trials,
the risks of lower glycemic targets may,
on a population level, outweigh the
potential benefits on microvascular
complications.
The concerning mortality findings in
the ACCORD trial, discussed below
(39), and the relatively intense efforts
required to achieve near-euglycemia
should also be considered when setting
glycemic targets. However, based on
physician judgment and patient prefer-
ences, select patients, especially those
with little comorbidity and long life ex-
pectancy, may benefit from adopting
Diabetes Care Volume 38, Supplement 1, January 2015
more intensive glycemic targets (e.g.,
A1C target ,6.5%) as long as signifi-
cant hypoglycemia does not become a
barrier.
A1C and Cardiovascular Disease
Outcomes
CVD is a more common cause of death
than microvascular complications in
populations with diabetes. There is evi-
dence for a cardiovascular benefit of in-
tensive glycemic control after long-term
follow-up of study cohorts treated early
in the course of type 1 and type 2 di-
abetes. In the DCCT, there was a trend
toward lower risk of CVD events with
intensive control. In the 9-year post-
DCCT follow-up of the EDIC cohort, par-
ticipants previously randomized to the
intensive arm had a significant 57% re-
duction in the risk of nonfatal myocar-
dial infarction (MI), stroke, or CVD
death compared with those previously
in the standard arm (40). The benefit of
intensive glycemic control in this type 1
diabetic cohort has recently been
shown to persist for several decades
(41).
In type 2 diabetes, there is evidence
that more intensive treatment of
glycemia in newly diagnosed patients
may reduce long-term CVD rates. Dur-
ing the UKPDS trial, there was a 16%
reduction in CVD events (combined
fatal or nonfatal MI and sudden death)
in the intensive glycemic control
arm that did not reach statistical sig-
nificance (P 5 0.052), and there was
no suggestion of benefit on other
CVD outcomes (e.g., stroke). However,
after 10 years of follow-up, those orig-
inally randomized to intensive glyce-
mic control had significant long-term
reductions in MI (15% with sulfo-
nylurea or insulin as initial pharmaco-
therapy, 33% with metformin as initial
pharmacotherapy) and in all-cause
mortality (13% and 27%, respectively)
(34).
The ACCORD, ADVANCE, and VADT
suggested no significant reduction in
CVD outcomes with intensive glycemic
control in participants followed for
3.525.6 years who had more advanced
type 2 diabetes than UKPDS partici-
pants. All three trials were conducted
in participants with more long-standing
diabetes (mean duration 8–11 years)
and either known CVD or multiple car-
diovascular risk factors. The target A1C
among intensive control subjects was
,6% in ACCORD, ,6.5% in ADVANCE,
and a 1.5% reduction in A1C compared
with control subjects in VADT. Details of
these studies are reviewed extensively
in the ADA position statement “Intensive
Glycemic Control and the Prevention
of Cardiovascular Events: Implications
of the ACCORD, ADVANCE, and VA
Diabetes Trials: A Position Statement
of the American Diabetes Association
and a Scientific Statement of the
American College of Cardiology Foun-
dation and the American Heart
Association” (42).
The glycemic control comparison in
ACCORD was halted early due to an
increased mortality rate in the inten-
sive compared with the standard
arm (1.41% vs. 1.14% per year; hazard
ratio 1.22 [95% CI 1.01–1.46]), with a
similar increase in cardiovascular
deaths.
Key Points
1. Analysis of the ACCORD data did not
identify a clear explanation for the
excess mortality in the intensive
arm (39).
2. A group-level meta-analysis of
ACCORD, ADVANCE, and VADT
suggested that glucose lowering
had a modest (9%) but statisti-
cally significant reduction in major
CVD outcomes, primarily nonfatal
MI, with no significant effect on
mortality.
3. Heterogeneity of the mortality ef-
fects across studies was noted.
4. A prespecified subgroup analy-
sis suggested that major CVD
outcome reduction occurred in pa-
tients without known CVD at base-
line (hazard ratio 0.84 [95% CI
0.74–0.94]) (43).
5. Mortality findings in ACCORD (39)
and subgroup analyses of the VADT
(44) suggested that the potential
risks of intensive glycemic control
may outweigh its benefits in some
patients.
6. Those with long duration of diabetes,
known history of severe hypoglyce-
mia, advanced atherosclerosis, or ad-
vanced age/frailty may benefit from
less aggressive targets.
7. Severe hypoglycemia was signifi-
cantly more likely in participants in
all three trials randomized to the in-
tensive glycemic control arm.
care.diabetesjournals.org Position Statement S37

Table 6.2—Summary of glycemic recommendations for nonpregnant adults with targeting postprandial glucose com-
diabetes pared with those targeting prepran-
A1C ,7.0%* dial glucose (48). Therefore, it is
Preprandial capillary plasma glucose 80–130 mg/dL* (4.4–7.2 mmol/L) reasonable for postprandial testing
Peak postprandial capillary plasma glucose† ,180 mg/dL* (,10.0 mmol/L) to be recommended for individuals
*More or less stringent glycemic goals may be appropriate for individual patients. Goals should
who have premeal glucose values
be individualized based on duration of diabetes, age/life expectancy, comorbid conditions, within target but have A1C values
known CVD or advanced microvascular complications, hypoglycemia unawareness, and above target. Taking postprandial
individual patient considerations. plasma glucose measurements 1–2 h
†Postprandial glucose may be targeted if A1C goals are not met despite reaching preprandial
glucose goals. Postprandial glucose measurements should be made 1–2 h after the beginning of after the start of a meal and using
the meal, generally peak levels in patients with diabetes. treatments aimed at reducing post-
prandial plasma glucose values to
,180 mg/dL (10 mmol/L) may help
lower A1C.
Providers sh oul d be v ig il an t i n negatively affected by postprandial An analysis of data from 470 par-
preventing severe hypoglycemia in hyperglycemia (47). It is clear that post- ticipants of the ADAG study (237
patients with advanced disease and prandial hyperglycemia, like prepran- with type 1 diabetes and 147 with
should not aggressively attempt to dial hyperglycemia, contributes to type 2 diabetes) found that actual
achieve near-normal A1C levels in pa- elevated A1C levels, with its relative average glucose levels associated
tients in whom such targets cannot be contribution being greater at A1C levels with conventional A1C targets were
safely and reasonably achieved. Severe that are closer to 7%. However, outcome higher than older DCCT and ADA
or frequent hypoglycemia is an abso- studies have clearly shown A1C to be targets (Table 6.1) (21,25). These find-
lute indication for the modification of the primary predictor of complications, ings support that premeal glucose
treatment regimens, including setting and landmark glycemic control trials targets may be relaxed without un-
higher glycemic goals. Many factors, such as the DCCT and UKPDS relied dermining overall glycemic control as
including patient preferences, should overwhelmingly on preprandial SMBG. measured by A1C. These data have
be taken into account when develop- Additionally, a randomized controlled prompted a revision in the ADA-
ing a patient’s individualized goals trial in patients with known CVD found recommended premeal target to 80–
(Table 6.2). no CVD benefit of insulin regimens 130 mg/dL (4.4–7.2 mmol/L).

A1C and Glycemic Targets

Numerous aspects must be considered
when setting glycemic targets. The
ADA proposes optimal targets, but
each target must be individualized to
the needs of each patient and their
disease factors. When possible, such
decisions should be made with the
patient, reflecting his or her preferences,
needs, and values. Figure 6.1 is not
designed to be applied rigidly but used
as a broad construct to guide clinical
decision making (45), both in type 1
and type 2 diabetes.
Recommended glycemic targets for
many nonpregnant adults are shown
in Table 6.2. The recommendations
include blood glucose levels that ap-
pear to correlate with achievement of
an A1C of ,7%. The issue of prepran-
dial versus postprandial SMBG targets
is complex (46). Elevated postchal-
lenge (2-h oral glucose tolerance
test) glucose values have been associ-
ated with increased cardiovascular
risk independent of fasting plasma glu-
cose in some epidemiological studies.
Figure 6.1—Depicted are patient and disease factors used to determine optimal A1C targets.
In subjects with diabetes, surrogate Characteristics and predicaments toward the left justify more stringent efforts to lower A1C;
measures of vascular pathology, such those toward the right suggest less stringent efforts. Adapted with permission from Inzucchi
as endothelial dysfunction, are et al. (45).
S38 Position Statement
HYPOGLYCEMIA
Recommendations
c Individuals at risk for hypoglycemia
should be asked about symptom-
atic and asymptomatic hypoglyce-
mia at each encounter. C
c Glucose (15–20 g) is the preferred
treatment for the conscious individ-
ual with hypoglycemia, although any
form of carbohydrate that contains
glucose may be used. Fifteen minutes
after treatment, if SMBG shows con-
tinued hypoglycemia, the treatment
should be repeated. Once SMBG re-
turns to normal, the individual should
consume a meal or snack to prevent
recurrence of hypoglycemia. E
c Glucagon should be prescribed for
all individuals at an increased risk of
severe hypoglycemia, and care-
givers or family members of these
individuals should be instructed on
its administration. Glucagon admin-
istration is not limited to health
care professionals. E
c Hypoglycemia unawareness or one
or more episodes of severe hypo-
glycemia should trigger reevalua-
tion of the treatment regimen. E
c Insulin-treated patients with hypo-
glycemia unawareness or an episode
of severe hypoglycemia should be
advised to raise their glycemic tar-
gets to strictly avoid further hypogly-
cemia for at least several weeks in
order to partially reverse hypoglyce-
mia unawareness and reduce risk of
future episodes. A
c Ongoing assessment of cognitive
function is suggested with increased
vigilance for hypoglycemia by the cli-
nician, patient, and caregivers if low
cognition and/or declining cognition
is found. B
Hypoglycemia is the leading limiting fac-
tor in the glycemic management of type
1 and insulin-treated type 2 diabetes
(49). Mild hypoglycemia may be incon-
venient or frightening to patients with
diabetes. Severe hypoglycemia can
cause acute harm to the person with di-
abetes or others, especially if it causes
falls, motor vehicle accidents, or other
injury. A large cohort study suggested
that among older adults with type 2
diabetes, a history of severe hypoglycemia
was associated with greater risk of
Diabetes Care Volume 38, Supplement 1, January 2015
dementia (50). Conversely, in a substudy
of the ACCORD trial, cognitive impair-
ment at baseline or decline in cognitive
function during the trial was significantly
associated with subsequent episodes of
severe hypoglycemia (51). Evidence from
the DCCT/EDIC, which involved younger
adults and adolescents with type 1 diabe-
tes, found no association between fre-
quency of severe hypoglycemia and
cognitive decline (52), as discussed in
Section 11. Children and Adolescents.
Severe hypoglycemia was associated
with mortality in participants in both the
standard and intensive glycemia arms
of the ACCORD trial, but the relation-
ships between hypoglycemia, achieved
A1C, and treatment intensity were not
straightforward. An association of severe
hypoglycemia with mortality was also
found in the ADVANCE trial (53). An asso-
ciation between self-reported severe hy-
poglycemia and 5-year mortality has also
been reported in clinical practice (54).
In 2013, the ADA and the Endocrine
Society published the consensus report
“Hypoglycemia and Diabetes: A Report
of a Workgroup of the American Diabe-
tes Association and the Endocrine Soci-
ety” (55) on the effect and treatment of
hypoglycemia in patients with diabetes.
Severe hypoglycemia was defined as an
event requiring the assistance of an-
other person. Young children with type
1 diabetes and the elderly were noted
as particularly vulnerable due to their
limited ability to recognize hypogly-
cemic symptoms and effectively com-
municate their needs. Individualized
patient education, dietary interven-
tion (e.g., bedtime snack to prevent
overnight hypoglycemia), exercise
management, medication adjustment,
glucose monitoring, and routine clini-
cal surveillance may improve patient
outcomes.
Hypoglycemia Treatment
Hypoglycemia treatment requires inges-
tion of glucose- or carbohydrate-
containing foods. The acute glycemic
response correlates better with the glu-
cose content of food than with the car-
bohydrate content of food. Pure glucose
is the preferred treatment, but any form
of carbohydrate that contains glucose
will raise blood glucose. Added fat may
retard and then prolong the acute gly-
cemic response. Ongoing insulin activity
or insulin secretagogues may lead to
recurrent hypoglycemia unless further
food is ingested after recovery.
Glucagon
Those in close contact with, or having cus-
todial care of, people with hypoglycemia-
prone diabetes (family members,
roommates, school personnel, child care
providers, correctional institution staff, or
coworkers) should be instructed on the
use of glucagon kits. An individual does
not need to be a health care professional
to safely administer glucagon. A glucagon
kit requires a prescription. Care should be
taken to ensure that glucagon kits are not
expired.
Hypoglycemia Prevention
Hypoglycemia prevention is a critical
component of diabetes management.
SMBG and, for some patients, CGM are
essential tools to assess therapy and de-
tect incipient hypoglycemia. Patients
should understand situations that
increase their risk of hypoglycemia,
such as fasting for tests or procedures,
during or after intense exercise, and
during sleep. Hypoglycemia may in-
crease the risk of harm to self or others,
such as with driving. Teaching people
with diabetes to balance insulin use
and carbohydrate intake and exercise
are necessary, but these strategies are
not always sufficient for prevention.
In type 1 diabetes and severely
insulin-deficient type 2 diabetes, hypo-
glycemia unawareness (or hypoglycemia-
associated autonomic failure) can
severely compromise stringent diabe-
tes control and quality of life. This syn-
drome is characterized by deficient
counterregulatory hormone release, es-
pecially in older adults, and a dimin-
ished autonomic response, which both
are risk factors for, and caused by, hy-
poglycemia. A corollary to this “vicious
cycle” is that several weeks of avoid-
ance of hypoglycemia has been demon-
strated to improve counterregulation
and awareness to some extent in
many patients (56). Hence, patients
with one or more episodes of severe
hypoglycemia may benefit from at least
short-term relaxation of glycemic
targets.
INTERCURRENT ILLNESS
For further information on management
of patients with hyperglycemia in the
hospital, please refer to Section 13. Di-
abetes Care in the Hospital, Nursing
care.diabetesjournals.org
Home, and Skilled Nursing Facility.
Stressful events (e.g., illness, trauma,
surgery, etc.) frequently aggravate
glycemic control and may precipitate
diabetic ketoacidosis or nonketotic hy-
perosmolar state, life-threatening con-
ditions that require immediate medical
care to prevent complications and death.
Any condition leading to deterioration in
glycemic control necessitates more fre-
quent monitoring of blood glucose;
ketosis-prone patients also require urine
or blood ketone monitoring. If accompa-
nied by ketosis, vomiting, or alteration in
level of consciousness, marked hypergly-
cemia requires temporary adjustment of
the treatment regimen and immediate
interaction with the diabetes care
team. The patient treated with noninsu-
lin therapies or medical nutrition ther-
apy alone may temporarily require
insulin. Adequate fluid and caloric intake
must be assured. Infection or dehydra-
tion is more likely to necessitate hospi-
talization of the person with diabetes
than the person without diabetes.
A physician with expertise in diabetes
management should treat the hospital-
ized patient. For further information on
diabetic ketoacidosis management or hy-
perglycemic nonketotic hyperosmolar
state, please refer to the ADA statement
“Hyperglycemic Crises in Adult Patients
With Diabetes” (57).
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37. Ismail-Beigi F, Craven T, Banerji MA, et al.;
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38. Adler AI, Stratton IM, Neil HAW, et al. As-
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1335–1343
Diabetes Care Volume 38, Supplement 1, January 2015 S41

American Diabetes Association

7. Approaches to Glycemic
Treatment
Diabetes Care 2015;38(Suppl. 1):S41–S48 | DOI: 10.2337/dc15-S010

PHARMACOLOGICAL THERAPY FOR TYPE 1 DIABETES

Recommendations
c Most people with type 1 diabetes should be treated with multiple-dose insulin
(MDI) injections (three to four injections per day of basal and prandial insulin)
or continuous subcutaneous insulin infusion (CSII). A
c Most people with type 1 diabetes should be educated in how to match pran-
dial insulin dose to carbohydrate intake, premeal blood glucose, and antici-
pated activity. E

POSITION STATEMENT
c Most people with type 1 diabetes should use insulin analogs to reduce hypo-
glycemia risk. A

Insulin Therapy
There are excellent reviews to guide the initiation and management of insulin
therapy to achieve desired glycemic goals (1,2,3). Although most studies of MDI
versus pump therapy have been small and of short duration, a systematic review and
meta-analysis concluded that there were no systematic differences in A1C or severe
hypoglycemia rates in children and adults between the two forms of intensive in-
sulin therapy (4). A large randomized trial in type 1 diabetic patients with nocturnal
hypoglycemia reported that sensor-augmented insulin pump therapy with the
threshold suspend feature reduced nocturnal hypoglycemia, without increasing
glycated hemoglobin values (5). Overall, intensive management through pump
therapy/continuous glucose monitoring and active patient/family participation
should be strongly encouraged (6–8). For selected individuals who have mastered
carbohydrate counting, education on the impact of protein and fat on glycemic
excursions can be incorporated into diabetes management (9).
The Diabetes Control and Complications Trial (DCCT) clearly showed that intensive
insulin therapy (three or more injections per day of insulin) or CSII (insulin pump therapy)
was a key part of improved glycemia and better outcomes (10,11). The study was carried
out with short- and intermediate-acting human insulins. Despite better microvascular
outcomes, intensive insulin therapy was associated with a high rate of severe hypogly-
cemia (62 episodes per 100 patient-years of therapy). Since the DCCT, a number of rapid-
acting and long-acting insulin analogs have been developed. These analogs are associated
with less hypoglycemia in type 1 diabetes, while matching the A1C lowering of human
insulins (1,12).

Recommended therapy for type 1 diabetes consists of the following:

1. Use MDI injections (three to four injections per day of basal and prandial insulin)
or CSII therapy.
2. Match prandial insulin to carbohydrate intake, premeal blood glucose, and an-
ticipated physical activity.
3. For most patients (especially those at an elevated risk of hypoglycemia), use Suggested citation: American Diabetes Associa-
insulin analogs. tion. Approaches to glycemic treatment. Sec. 7.
4. For patients with frequent nocturnal hypoglycemia and/or hypoglycemia unawareness, In Standards of Medical Care in Diabetesd2015.
a sensor-augmented low glucose threshold suspend pump may be considered. Diabetes Care 2015;38(Suppl. 1):S41–S48
© 2015 by the American Diabetes Association.
Pramlintide Readers may use this article as long as the work
Pramlintide, an amylin analog, is an agent that delays gastric emptying, blunts is properly cited, the use is educational and not
pancreatic secretion of glucagon, and enhances satiety. It is a U.S. Food and Drug for profit, and the work is not altered.
S42 Position Statement
Administration (FDA)-approved therapy
for use in type 1 diabetes. It has been
shown to induce weight loss and lower
insulin dose; however, it is only indi-
cated in adults. Concurrent reduction
of prandial insulin dosing is required to
reduce the risk of severe hypoglycemia.
Investigational Agents
Metformin
Adding metformin to insulin therapy may
reduce insulin requirements and improve
metabolic control in overweight/obese
patients with poorly controlled type 1
diabetes. In a meta-analysis, metformin
in type 1 diabetes was found to reduce
insulin requirements (6.6 U/day, P ,
0.001) and led to small reductions in
weight and total and LDL cholesterol but
not to improved glycemic control (abso-
lute A1C reduction 0.11%, P 5 0.42) (13).
Incretin-Based Therapies
Therapies approved for the treatment of
type 2 diabetes are currently being eval-
uated in type 1 diabetes. Glucagon-like
peptide 1 (GLP-1) agonists and dipep-
tidyl peptidase 4 (DPP-4) inhibitors are
not currently FDA approved for those
with type 1 diabetes, but are being stud-
ied in this population.
Sodium–Glucose Cotransporter 2 Inhibitors
Sodium–glucose cotransporter 2 (SGLT2)
inhibitors provide insulin-independent
glucose lowering by blocking glucose
reabsorption in the proximal renal tubule
by inhibiting SGLT2. These agents provide
modest weight loss and blood pressure
reduction. Although there are two FDA-
approved agents for use in patients with
type 2 diabetes, there are insufficient
data to recommend clinical use in type 1
diabetes at this time (14).
PHARMACOLOGICAL THERAPY FOR
TYPE 2 DIABETES
Recommendations
c Metformin, if not contraindicated
and if tolerated, is the preferred
initial pharmacological agent for
type 2 diabetes. A
c In patients with newly diagnosed
type 2 diabetes and markedly symp-
tomatic and/or elevated blood glu-
cose levels or A1C, consider initiating
insulin therapy (with or without
additional agents). E
c If noninsulin monotherapy at max-
imum tolerated dose does not
Diabetes Care Volume 38, Supplement 1, January 2015
achieve or maintain the A1C target
over 3 months, add a second oral
agent, a GLP-1 receptor agonist, or
basal insulin. A
c A patient-centered approach
should be used to guide choice
of pharmacological agents. Con-
siderations i nclude ef fic a cy,
cost, potential side effects, weight,
comorbidities, hypoglycemia risk,
and patient preferences. E
c Due to the progressive nature of
type 2 diabetes, insulin therapy is
eventually indicated for many pa-
tients with type 2 diabetes. B
An updated American Diabetes Asso-
ciation/European Association for the
Study of Diabetes position statement
(15) evaluated the data and developed
recommendations, including advan-
tages and disadvantages, for antihyper-
glycemic agents for type 2 diabetic
patients. A patient-centered approach
is stressed, including patient prefer-
ences, cost and potential side effects
of each class, effects on body weight,
and hypoglycemia risk. Lifestyle modifi-
cations that improve health (see Section
4. Foundations of Care) should be em-
phasized along with any pharmacologi-
cal therapy.
Initial Therapy
Most patients should begin with life-
style changes (lifestyle counseling,
weight-loss education, exercise, etc.).
When lifestyle efforts alone have not
achieved or maintained glycemic goals,
metformin monotherapy should be
added at, or soon after, diagnosis, un-
less there are contraindications or intol-
erance. Metformin has a long-standing
evidence base for efficacy and safety, is
inexpensive, and may reduce risk of car-
diovascular events (16). In patients with
metformin intolerance or contraindica-
tions, consider an initial drug from other
classes depicted in Fig. 7.1 under “Dual
therapy” and proceed accordingly.
Combination Therapy
Although there are numerous trials
comparing dual therapy with metformin
alone, few directly compare drugs as
add-on therapy. A comparative effec-
tiveness meta-analysis (17) suggests
that overall each new class of noninsulin
agents added to initial therapy lowers
A1C around 0.9–1.1%. A comprehensive
listing, including the cost, is available in
Table 7.1.
If the A1C target is not achieved after
approximately 3 months, consider a
combination of metformin and one of
these six treatment options: sulfonyl-
urea, thiazolidinedione, DPP-4 inhibi-
tors, SGLT2 inhibitors, GLP-1 receptor
agonists, or basal insulin (Fig. 7.1).
Drug choice is based on patient prefer-
ences as well as various patient, disease,
and drug characteristics, with the goal of
reducing blood glucose levels while
minimizing side effects, especially hypo-
glycemia. Figure 7.1 emphasizes drugs
commonly used in the U.S. and/or Europe.
Rapid-acting secretagogues (megliti-
nides) may be used instead of sulfonyl-
ureas in patients with irregular meal
schedules or who develop late post-
prandial hypoglycemia on a sulfonyl-
urea. Other drugs not shown in the
figure (e.g., a-glucosidase inhibitors, co-
lesevelam, bromocriptine, pramlintide)
may be tried in specific situations, but
are generally not favored due to modest
efficacy, the frequency of administra-
tion, and/or side effects.
For all patients, consider initiating
therapy with a dual combination when
A1C is $9% to more expeditiously
achieve the target A1C level. Insulin
has the advantage of being effective
where other agents may not be and
should be considered as part of any
combination regimen when hyperglyce-
mia is severe, especially if symptoms are
present or any catabolic features
(weight loss, ketosis) are in evidence.
Consider initiating combination insulin
injectable therapy when blood glucose
is $300–350 mg/dL (16.7–19.4 mmol/L)
and/or A1C is $10–12%. As the pa-
tient’s glucose toxicity resolves, the
regimen can, potentially, be subse-
quently simplified.
Insulin Therapy
Many patients with type 2 diabetes even-
tually require and benefit from insulin
therapy. Providers may wish to consider
regimen flexibility when devising a plan
for the initiation and adjustment of insu-
lin therapy in people with type 2 diabetes
(Fig. 7.2). The progressive nature of type
2 diabetes and its therapies should be
regularly and objectively explained to pa-
tients. Providers should avoid using insu-
lin as a threat or describing it as a failure
care.diabetesjournals.org Position Statement S43

Figure 7.1—Antihyperglycemic therapy in type 2 diabetes: general recommendations (15). The order in the chart was determined by historical
availability and the route of administration, with injectables to the right; it is not meant to denote any specific preference. Potential sequences of
antihyperglycemic therapy for patients with type 2 diabetes are displayed, with the usual transition moving vertically from top to bottom (although
horizontal movement within therapy stages is also possible, depending on the circumstances). DPP-4-i, DPP-4 inhibitor; fxs, fractures; GI, gastro-
intestinal; GLP-1-RA, GLP-1 receptor agonist; GU, genitourinary; HF, heart failure; Hypo, hypoglycemia; SGLT2-i, SGLT2 inhibitor; SU, sulfonylurea;
TZD, thiazolidinedione. *See ref. 15 for description of efficacy categorization. †Consider starting at this stage when A1C is $9%. ‡Consider starting at
this stage when blood glucose is $300–350 mg/dL (16.7–19.4 mmol/L) and/or A1C is $10–12%, especially if symptomatic or catabolic features are
present, in which case basal insulin 1 mealtime insulin is the preferred initial regimen. §Usually a basal insulin (NPH, glargine, detemir, degludec).
Adapted with permission from Inzucchi et al. (15).

or punishment. Equipping patients with
an algorithm for self-titration of insulin
doses based on self-monitoring of blood
glucose (SMBG) improves glycemic con-
trol in type 2 diabetic patients initiating
insulin (18).
Basal insulin alone is the most conve-
nient initial insulin regimen, beginning
at 10 U or 0.1–0.2 U/kg, depending on
the degree of hyperglycemia. Basal in-
sulin is usually prescribed in conjunction
with metformin and possibly one addi-
tional noninsulin agent. If basal insulin
has been titrated to an acceptable fast-
ing blood glucose level, but A1C remains
above target, consider advancing to
combination injectable therapy (Fig. 7.2)
to cover postprandial glucose excur-
sions. Options include adding a GLP-1
receptor agonist or mealtime insulin,
consisting of one to three injections of
rapid-acting insulin analog (lispro, as-
part, or glulisine) administered just be-
fore eating. A less studied alternative,
transitioning from basal insulin to
twice-daily premixed (or biphasic) insu-
lin analog (70/30 aspart mix, 75/25
or 50/50 lispro mix), could also be con-
sidered. Regular human insulin and
human NPH-Regular premixed formula-
tions (70/30) are less costly alternatives
to rapid-acting insulin analogs and
premixed insulin analogs, respectively,
but their pharmacodynamic profiles
make them suboptimal for the coverage
of postprandial glucose excursions. A
less commonly used and more costly
alternative to “basal–bolus” therapy
with multiple daily injections is CSII
(insulin pump). In addition to the sug-
gestions provided for determining
the starting dose of mealtime insulin
under a basal–bolus regimen, another
method consists of adding up the total
current insulin dose and then providing
one-half of this amount as basal and
one-half as mealtime insulin, the latter
split evenly between three meals.
 S44

Table 7.1—Properties of available glucose-lowering agents in the U.S. and Europe that may guide individualized treatment choices in patients with type 2 diabetes (15)
Class Compound(s) Cellular mechanism(s) Primary physiological action(s) Advantages Disadvantages Cost*
Biguanides c Metformin Activates AMP-kinase c ↓ Hepatic glucose production c Extensive experience c Gastrointestinal side effects (diarrhea, Low
Position Statement

(? other) c No hypoglycemia abdominal cramping)

c ↓ CVD events (UKPDS) c Lactic acidosis risk (rare)
c Vitamin B12 deficiency
c Multiple contraindications: CKD,
acidosis, hypoxia, dehydration, etc.
Sulfonylureas 2nd Generation Closes KATP channels on c ↑ Insulin secretion c Extensive experience c Hypoglycemia Low
c Glyburide/glibenclamide b-cell plasma membranes c ↓ Microvascular risk c ↑ Weight
c Glipizide (UKPDS) c ? Blunts myocardial ischemic
c Gliclazide† preconditioning
c Glimepiride c Low durability
Meglitinides c Repaglinide Closes KATP channels on c ↑ Insulin secretion c ↓Postprandial glucose c Hypoglycemia Moderate
(glinides) c Nateglinide b-cell plasma membranes excursions c ↑ Weight
c Dosing flexibility c ? Blunts myocardial ischemic
preconditioning
c Frequent dosing schedule
TZDs c Pioglitazone‡ Activates the nuclear c ↑ Insulin sensitivity c No hypoglycemia c ↑ Weight Low
c Rosiglitazone§ transcription factor PPAR-g c Durability c Edema/heart failure
c ↑ HDL-C c Bone fractures
c ↓ Triglycerides c ↑ LDL-C (rosiglitazone)
(pioglitazone) c ? ↑ MI (meta-analyses, rosiglitazone)
c ? ↓ CVD events
(PROactive,
pioglitazone)
a-Glucosidase c Acarbose Inhibits intestinal c Slows intestinal carbohydrate c No hypoglycemia c Generally modest A1C efficacy Moderate
inhibitors c Miglitol a-glucosidase digestion/absorption c ↓Postprandial glucose c Gastrointestinal side effects
excursions (flatulence, diarrhea)
c ? ↓ CVD events c Frequent dosing schedule
(STOP-NIDDM)
c Nonsystemic
DPP-4 inhibitors c Sitagliptin Inhibits DPP-4 activity, c ↑ Insulin secretion c No hypoglycemia c Angioedema/urticaria and other High
c Vildagliptin† increasing postprandial (glucose-dependent) c Well tolerated immune-mediated dermatological
c Saxagliptin active incretin (GLP-1, GIP) c ↓ Glucagon secretion effects
c Linagliptin concentrations (glucose-dependent) c ? Acute pancreatitis
c Alogliptin c ? ↑ Heart failure hospitalizations
Bile acid c Colesevelam Binds bile acids in c ? ↓ Hepatic glucose c No hypoglycemia c Generally modest A1C efficacy High
sequestrants intestinal tract, increasing production c ↓ LDL-C c Constipation
hepatic bile acid c ? ↑ Incretin levels c ↑ Triglycerides
production c May ↓ absorption of other medications

Continued on p. S45
Diabetes Care Volume 38, Supplement 1, January 2015
Table 7.1—Continued
Class Compound(s) Cellular mechanism(s) Primary physiological action(s) Advantages Disadvantages Cost*
Dopamine-2 c Bromocriptine (quick release)§ Activates dopaminergic c Modulates hypothalamic c No hypoglycemia c Generally modest A1C efficacy High
agonists receptors regulation of metabolism c ? ↓ CVD events c Dizziness/syncope
c ↑ Insulin sensitivity (Cycloset Safety Trial) c Nausea
c Fatigue
c Rhinitis
care.diabetesjournals.org

SGLT2 inhibitors c Canagliflozin Inhibits SGLT2 in the c Blocks glucose reabsorption c No hypoglycemia c Genitourinary infections High
c Dapagliflozin‡ proximal nephron by the kidney, increasing c ↓ Weight c Polyuria
c Empagliflozin glucosuria c ↓ Blood pressure c Volume depletion/hypotension/
c Effective at all stages dizziness
of T2DM c ↑ LDL-C
c ↑ Creatinine (transient)
GLP-1 receptor c Exenatide Activates GLP-1 receptors c ↑ Insulin secretion (glucose- c No hypoglycemia c Gastrointestinal side effects (nausea/ High
agonists c Exenatide extended release dependent) c ↓ Weight vomiting/diarrhea)
c Liraglutide c ↓ Glucagon secretion c ↓ Postprandial glucosec ↑ Heart rate
c Albiglutide (glucose-dependent) excursions c ? Acute pancreatitis
c Lixisenatide† c Slows gastric emptying c ↓ Some cardiovascular c C-cell hyperplasia/medullary thyroid
c Dulaglutide c ↑ Satiety risk factors tumors in animals
c Injectable
c Training requirements
Amylin mimetics c Pramlintide§ Activates amylin receptors c ↓ Glucagon secretion c ↓ Postprandial glucose c Generally modest A1C efficacy High
c Slows gastric emptying excursions c Gastrointestinal side effects (nausea/
c ↑ Satiety c ↓ Weight vomiting)
c Hypoglycemia unless insulin dose is
simultaneously reduced
c Injectable
c Frequent dosing schedule
c Training requirements
Insulins c Rapid-acting analogs Activates insulin receptors c ↑ Glucose disposal c Nearly universal c Hypoglycemia Variable#
- Lispro c ↓ Hepatic glucose production response c Weight gain
- Aspart c Other c Theoretically unlimited c ? Mitogenic effects
- Glulisine efficacy c Injectable
c Short-acting c ↓ Microvascular risk c Patient reluctance
- Human Regular (UKPDS) c Training requirements
c Intermediate-acting
- Human NPH
c Basal insulin analogs
- Glargine
- Detemir
- Degludec†
c Premixed (several types)

CKD, chronic kidney disease; CVD, cardiovascular disease; GIP, glucose-dependent insulinotropic peptide; HDL-C, HDL cholesterol; LDL-C, LDL cholesterol; MI, myocardial infarction; PPAR-g, peroxisome
proliferator–activated receptor g; PROactive, Prospective Pioglitazone Clinical Trial in Macrovascular Events (30); STOP-NIDDM, Study to Prevent Non-Insulin-Dependent Diabetes Mellitus (31); TZD,
thiazolidinedione; T2DM, type 2 diabetes mellitus; UKPDS, UK Prospective Diabetes Study (32,33). Cycloset trial of quick-release bromocriptine (34). *Cost is based on lowest-priced member of the class (see ref.
15). †Not licensed in the U.S. ‡Initial concerns regarding bladder cancer risk are decreasing after subsequent study. §Not licensed in Europe for type 2 diabetes. #Cost is highly dependent on type/brand (analogs .
human insulins) and dosage. Adapted with permission from Inzucchi et al. (15).
Position Statement
S45
S46 Position Statement
Figure 7.2—Approach to starting and adjusting insulin in type 2 diabetes (15). FBG, fasting blood glucose; GLP-1-RA, GLP-1 receptor agonist; hypo,
hypoglycemia; mod., moderate; PPG, postprandial glucose; #, number. Adapted with permission from Inzucchi et al. (15).
Figure 7.2 focuses solely on sequen-
tial insulin strategies, describing the
number of injections and the relative
complexity and flexibility of each stage.
Once an insulin regimen is initiated,
dose titration is important, with adjust-
ments made in both mealtime and basal
insulins based on the prevailing blood
glucose levels and an understanding of
the pharmacodynamic profile of each
formulation (pattern control).
Noninsulin agents may be continued,
although sulfonylureas, DPP-4 inhibitors,
and GLP-1 receptor agonists are typically
stopped once more complex insulin regi-
mens beyond basal are used. In patients
with suboptimal blood glucose control,
especially those requiring increasing insu-
lin doses, adjunctive use of thiazolidine-
diones (usually pioglitazone) or SGLT2
Diabetes Care Volume 38, Supplement 1, January 2015
inhibitors may be helpful in improving
need lifelong lifestyle support
control and reducing the amount of in-
and medical monitoring. B
sulin needed. Comprehensive educa-
c Although small trials have shown
tion regarding SMBG, diet, exercise,
glycemic benefit of bariatric surgery
and the avoidance of and response to
in patients with type 2 diabetes and
hypoglycemia are critically important in
BMI 30–35 kg/m2, there is currently
any patient using insulin.
insufficient evidence to generally
BARIATRIC SURGERY recommend surgery in patients
with BMI ,35 kg/m2. E
Recommendations
c Bariatric surgery may be con-
Bariatric and metabolic surgeries,
sidered for adults with BMI .35
either gastric banding or procedures
kg/m2 and type 2 diabetes, espe-
that involve resecting, bypassing, or
cially if diabetes or associated co-
transposing sections of the stomach
morbidities are difficult to control
and small intestine, can be effective
with lifestyle and pharmacological
weight-loss treatments for severe
therapy. B
obesity when performed as part of a
c Patients with type 2 diabetes who
comprehensive weight-management
have undergone bariatric surgery
program with lifelong lifestyle support
care.diabetesjournals.org
and medical monitoring. National guide-
lines support consideration for bariatric
surgery for people with type 2 diabetes
with BMI .35 kg/m2.
Advantages
Treatment with bariatric surgery has
been shown to achieve near- or com-
plete normalization of glycemia 2 years
following surgery in 72% of patients
(compared with 16% in a matched con-
trol group treated with lifestyle and
pharmacological interventions) (19). A
study evaluated the long-term (3-year)
outcomes of surgical intervention
(Roux-en-Y gastric bypass or sleeve gas-
trectomy) and intensive medical ther-
apy (quarterly visits, pharmacological
therapy, SMBG, diabetes education, life-
style counseling, and encouragement to
participate in Weight Watchers) com-
pared with just intensive medical ther-
apy on achieving a target A1C #6%
among obese patients with uncon-
trolled type 2 diabetes (mean A1C
9.3%). This A1C target was achieved by
38% (P , 0.001) in the gastric bypass
group, 24% (P 5 0.01) in the sleeve gas-
trectomy group, and 5% in those receiv-
ing medical therapy (20). Diabetes
remission rates tend to be higher with
procedures that bypass portions of the
small intestine and lower with proce-
dures that only restrict the stomach.
Younger age, shorter duration of type
2 diabetes, lower A1C, higher serum in-
sulin levels, and nonuse of insulin have
all been associated with higher remis-
sion rates after bariatric surgery (21).
Although bariatric surgery has been
shown to improve the metabolic profiles
of morbidly obese patients with type 1
diabetes, the role of bariatric surgery in
such patients will require larger and lon-
ger studies (22).
Disadvantages
Bariatric surgery is costly and has asso-
ciated risks. Morbidity and mortality
rates directly related to the surgery
have decreased considerably in recent
years, with 30-day mortality rates now
0.28%, similar to those for laparoscopic
cholecystectomy (23). Outcomes vary
depending on the procedure and the
experience of the surgeon and center.
Longer-term concerns include vitamin
and mineral deficiencies, osteoporosis,
and rare but often severe hypoglycemia
from insulin hypersecretion. Cohort
studies attempting to match surgical
and nonsurgical subjects suggest that
the procedure may reduce longer-term
mortality rates (19). In contrast, a pro-
pensity score-adjusted analysis of older,
severely obese patients in Veterans Af-
fairs Medical Centers found that bariatric
surgery was not associated with de-
creased mortality compared with usual
care (mean follow-up 6.7 years) (24). Ret-
rospective analyses and modeling studies
suggest that bariatric surgery may be
cost-effective for patients with type 2
diabetes, but the results are largely de-
pendent on assumptions about the
long-term effectiveness and safety of
the procedures (25–27). Understanding
the long-term benefits and risks of bariat-
ric surgery in individuals with type 2 diabe-
tes, especially those who are not severely
obese, will require well-designed clinical
trials, with optimal medical therapy as
the comparator (28). Unfortunately, such
studies may not be feasible (29).
References
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apy in type 1 and type 2 diabetes mellitus: sci-
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Alexandria, VA, American Diabetes Association,
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3. Mooradian AD, Bernbaum M, Albert SG. Nar-
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4. Yeh H-C, Brown TT, Maruthur N, et al. Com-
parative effectiveness and safety of methods of
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ASPIRE In-Home Study Group. Threshold-based
insulin-pump interruption for reduction of hy-
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6. Wood JR, Miller KM, Maahs DM, et al.; T1D
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7. Kmietowicz Z. Insulin pumps improve control
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1 diabetes. BMJ 2013;347:f5154
8. Phillip M, Battelino T, Atlas E, et al. Nocturnal
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9. Wolpert HA, Atakov-Castillo A, Smith SA,
Steil GM. Dietary fat acutely increases glucose
concentrations and insulin requirements in
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intensive diabetes management. Diabetes Care
2013;36:810–816
Position Statement S47
10. The Diabetes Control and Complications
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and progression of long-term complications in
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11. Nathan DM, Cleary PA, Backlund J-YC, et al.;
Diabetes Control and Complications Trial/Epi-
demiology of Diabetes Interventions and Com-
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lar disease in patients with type 1 diabetes.
N Engl J Med 2005;353:2643–2653
12. Rosenstock J, Dailey G, Massi-Benedetti M,
Fritsche A, Lin Z, Salzman A. Reduced hypoglyce-
mia risk with insulin glargine: a meta-analysis
comparing insulin glargine with human NPH
insulin in type 2 diabetes. Diabetes Care 2005;
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13. Vella S, Buetow L, Royle P, Livingstone S,
Colhoun HM, Petrie JR. The use of metformin
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14. Chiang JL, Kirkman MS, Laffel LM, Peters AL;
Type 1 Diabetes Sourcebook Authors. Type 1
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15. Inzucchi SE, Bergenstal RM, Buse JB, et al.
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tes, 2015: a patient-centered approach. Update
to a position statement of the American Diabe-
tes Association and the European Association
for the Study of Diabetes. Diabetes Care 2015;
38:140–149
16. Holman RR, Paul SK, Bethel MA, Matthews
DR, Neil HA. 10-year follow-up of intensive glu-
cose control in type 2 diabetes. N Engl J Med
2008;359:1577–1589
17. Bennett WL, Maruthur NM, Singh S, et al.
Comparative effectiveness and safety of medi-
cations for type 2 diabetes: an update including
new drugs and 2-drug combinations. Ann Intern
Med 2011;154:602–613
18. Blonde L, Merilainen M, Karwe V, Raskin P;
TITRATE Study Group. Patient-directed titration
for achieving glycaemic goals using a once-daily
basal insulin analogue: an assessment of two dif-
ferent fasting plasma glucose targets - the TITRATE
study. Diabetes Obes Metab 2009;11:623–631
19. Sjöström L, Peltonen M, Jacobson P, et al.
Association of bariatric surgery with long-term
remission of type 2 diabetes and with microvas-
cular and macrovascular complications. JAMA
2014;311:2297–2304
20. Schauer PR, Bhatt DL, Kirwan JP, et al.;
STAMPEDE Investigators. Bariatric surgery
versus intensive medical therapy for diabetesd
3-year outcomes. N Engl J Med 2014;370:2002–
2013
21. Still CD, Wood GC, Benotti P, et al. Preop-
erative prediction of type 2 diabetes remission
after Roux-en-Y gastric bypass surgery: a retro-
spective cohort study. Lancet Diabetes Endocri-
nol 2014;2:38–45
22. Brethauer SA, Aminian A, Rosenthal RJ,
Kirwan JP, Kashyap SR, Schauer PR. Bariatric
surgery improves the metabolic profile of mor-
bidly obese patients with type 1 diabetes. Di-
abetes Care 2014;37:e51–e52
23. Buchwald H, Estok R, Fahrbach K, Banel D,
Sledge I. Trends in mortality in bariatric surgery:
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a systematic review and meta-analysis. Surgery
2007;142:621–632
24. Maciejewski ML, Livingston EH, Smith VA,
et al. Survival among high-risk patients after
bariatric surgery. JAMA 2011;305:2419–2426
25. Hoerger TJ, Zhang P, Segel JE, Kahn HS,
Barker LE, Couper S. Cost-effectiveness of bari-
atric surgery for severely obese adults with di-
abetes. Diabetes Care 2010;33:1933–1939
26. Makary MA, Clark JM, Shore AD, et al. Med-
ication utilization and annual health care costs
in patients with type 2 diabetes mellitus before
and after bariatric surgery. Arch Surg 2010;145:
726–731
27. Keating CL, Dixon JB, Moodie ML, Peeters A,
Playfair J, O’Brien PE. Cost-efficacy of surgically
induced weight loss for the management of
type 2 diabetes: a randomized controlled trial.
Diabetes Care 2009;32:580–584
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28. Wolfe BM, Belle SH. Long-term risks and
benefits of bariatric surgery: a research chal-
lenge. JAMA 2014;312:1792–1793
29. Courcoulas AP, Goodpaster BH, Eagleton JK,
et al. Surgical vs medical treatments for type 2
diabetes mellitus: a randomized clinical trial.
JAMA Surg 2014;149:707–715
30. Dormandy JA, Charbonnel B, Eckland DJ,
et al.; PROactive Investigators. Secondary pre-
vention of macrovascular events in patients
with type 2 diabetes in the PROactive Study
(PROspective pioglitAzone Clinical Trial In mac-
rovascular Events): a randomised controlled tri-
al. Lancet 2005;366:1279–1289
31. Chiasson JL, Gomis R, Hanefeld M, Josse RG,
Karasik A, Laakso M; STOP-NIDDM Trial
Research Group. The STOP-NIDDM Trial: an in-
ternational study on the efficacy of an alpha-
glucosidase inhibitor to prevent type 2 diabetes
in a population with impaired glucose tolerance:
rationale, design, and preliminary screening
data. Diabetes Care 1998;21:1720–1725
32. UK Prospective Diabetes Study (UKPDS)
Group. Intensive blood-glucose control with sul-
phonylureas or insulin compared with conven-
tional treatment and risk of complications in
patients with type 2 diabetes (UKPDS 33). Lan-
cet 1998;352:837–853
33. UK Prospective Diabetes Study (UKPDS)
Group. Effect of intensive blood-glucose control
with metformin on complications in overweight
patients with type 2 diabetes (UKPDS 34). Lan-
cet 1998;352:854–865
34. Gaziano JM, Cincotta AH, O’Connor CM,
et al. Randomized clinical trial of quick-release
bromocriptine among patients with type 2 di-
abetes on overall safety and cardiovascular out-
comes. Diabetes Care 2010;33:1503–1508
Diabetes Care Volume 38, Supplement 1, January 2015 S49

American Diabetes Association

8. Cardiovascular Disease and Risk
Management
Diabetes Care 2015;38(Suppl. 1):S49–S57 | DOI: 10.2337/dc15-S011

For prevention and management of diabetes complications in children and adoles-

cents, please refer to Section 11. Children and Adolescents.

Cardiovascular disease (CVD) is the major cause of morbidity and mortality for
individuals with diabetes and is the largest contributor to the direct and indirect
costs of diabetes. The common conditions coexisting with type 2 diabetes (e.g.,
hypertension and dyslipidemia) are clear risk factors for CVD, and diabetes
itself confers independent risk. Numerous studies have shown the efficacy of con-
trolling individual cardiovascular risk factors in preventing or slowing CVD in people

POSITION STATEMENT
with diabetes. Large benefits are seen when multiple risk factors are addressed
globally (1,2). There is evidence that measures of 10-year coronary heart disease (CHD)
risk among U.S. adults with diabetes have improved significantly over the past decade (3).

HYPERTENSION/BLOOD PRESSURE CONTROL

Recommendations
Screening and Diagnosis
c Blood pressure should be measured at every routine visit. Patients found to
have elevated blood pressure should have blood pressure confirmed on a
separate day. B
Goals
c People with diabetes and hypertension should be treated to a systolic blood
pressure (SBP) goal of ,140 mmHg. A
c Lower systolic targets, such as ,130 mmHg, may be appropriate for certain
individuals, such as younger patients, if they can be achieved without undue
treatment burden. C
c Individuals with diabetes should be treated to a diastolic blood pressure (DBP)
,90 mmHg. A
c Lower diastolic targets, such as ,80 mmHg, may be appropriate for certain
individuals, such as younger patients, if they can be achieved without undue
treatment burden. B
Treatment
c Patients with blood pressure .120/80 mmHg should be advised on lifestyle
changes to reduce blood pressure. B
c Patients with confirmed office-based blood pressure higher than 140/90
mmHg should, in addition to lifestyle therapy, have prompt initiation and
timely subsequent titration of pharmacological therapy to achieve blood pres-
sure goals. A
c Lifestyle therapy for elevated blood pressure consists of weight loss, if over-
weight or obese; a Dietary Approaches to Stop Hypertension (DASH)-style
dietary pattern including reducing sodium and increasing potassium intake;
Suggested citation: American Diabetes Associa-
moderation of alcohol intake; and increased physical activity. B
tion. Cardiovascular disease and risk manage-
c Pharmacological therapy for patients with diabetes and hypertension should ment. Sec. 8. In Standards of Medical Care in
comprise a regimen that includes either an ACE inhibitor or an angiotensin Diabetesd2015. Diabetes Care 2015;38(Suppl. 1):
receptor blocker (ARB). B If one class is not tolerated, the other should be S49–S57
substituted. C © 2015 by the American Diabetes Association.
c Multiple-drug therapy (including a thiazide diuretic and ACE inhibitor/ARB, at Readers may use this article as long as the work
maximal doses) is generally required to achieve blood pressure targets. B is properly cited, the use is educational and not
for profit, and the work is not altered.
S50 Position Statement
c If ACE inhibitors, ARBs, or diuretics
are used, serum creatinine/estimated
glomerular filtration rate (eGFR) and
serum potassium levels should be
monitored. E
c In pregnant patients with diabetes
and chronic hypertension, blood
pressure targets of 110–129/65–
79 mmHg are suggested in the
interest of optimizing long-term
maternal health and minimizing
impaired fetal growth. ACE inhibi-
tors and ARBs are contraindicated
during pregnancy. E
Hypertension is a common diabetes
comorbidity that affects the majority
of patients, with the prevalence de-
pending on type of diabetes, age, obe-
sity, and ethnicity. Hypertension is a
major risk factor for both CVD and mi-
crovascular complications. In type 1 di-
abetes, hypertension is often the result
of underlying nephropathy, while in
type 2 diabetes it usually coexists with
other cardiometabolic risk factors.
Screening and Diagnosis
Blood pressure measurement should be
done by a trained individual and follow
the guidelines established for the gen-
eral population: measurement in the
seated position, with feet on the floor
and arm supported at heart level, after 5
min of rest. Cuff size should be appro-
priate for the upper arm circumference.
Elevated values should be confirmed
on a separate day.
Home blood pressure self-monitoring
and 24-h ambulatory blood pressure
monitoring may provide evidence of
white coat hypertension, masked hyper-
tension, or other discrepancies between
office and “true” blood pressure. Stud-
ies in individuals without diabetes found
that home measurements may better
correlate with CVD risk than office
measurements (4,5). However, most of
the evidence of benefits of hypertension
treatment in people with diabetes is
based on office measurements.
Treatment Goals
Epidemiological analyses show that
blood pressure .115/75 mmHg is asso-
ciated with increased cardiovascular
event rates and mortality in individuals
with diabetes and that SBP .120 mmHg
predicts long-term end-stage renal dis-
ease. Randomized clinical trials have
Diabetes Care Volume 38, Supplement 1, January 2015
demonstrated the benefit (reduction of
CHD events, stroke, and diabetic kidney
disease) of lowering blood pressure to
,140 mmHg systolic and ,90 mmHg
diastolic in individuals with diabetes
(6). There is limited prespecified clinical
trial evidence for the benefits of lower
SBP or DBP targets (7). A meta-analysis
of randomized trials of adults with type
2 diabetes comparing intensive blood
pressure targets (upper limit of 130
mmHg systolic and 80 mmHg diastolic)
to standard targets (upper limit of 140–
160 mmHg systolic and 85–100 mmHg
diastolic) found no significant reduction
in mortality or nonfatal myocardial in-
farction (MI). There was a statistically
significant 35% relative risk (RR) reduc-
tion in stroke with intensive targets, but
the absolute risk reduction was only 1%,
and intensive targets were associated
with an increased risk for adverse events
such as hypotension and syncope (8).
Given the epidemiological relation-
ship between lower blood pressure
and better long-term clinical outcomes,
two landmark trials, Action to Control
Cardiovascular Risk in Diabetes (ACCORD)
and Action in Diabetes and Vascular
Disease: Preterax and Diamicron MR
Controlled Evaluation–Blood Pressure
(ADVANCE-BP), were conducted in the
past decade to examine the benefit of
tighter blood pressure control in pa-
tients with type 2 diabetes.
The ACCORD trial examined whether a
lower SBP of ,120 mmHg, in type 2 di-
abetic patients at high risk for CVD, pro-
vided greater cardiovascular protection
than an SBP level of 130–140 mmHg (9).
The study did not find a benefit in primary
end point (nonfatal MI, nonfatal stroke,
and cardiovascular death) comparing in-
tensive blood pressure treatment (goal
,120 mmHg, average blood pressure
achieved 5 119/64 mmHg on 3.4 medica-
tions) with standard treatment (average
blood pressure achieved 5 143/70 mmHg
on 2.1 medications). In ACCORD, there was
no benefit of aggressive blood pressure
lowering, despite the extra cost and efforts.
In ADVANCE, the active blood pres-
sure intervention arm (a single-pill,
fixed-dose combination of perindopril
and indapamide) showed a significant
reduction in the risk of the primary com-
posite end point (major macrovascular
or microvascular event), as well as sig-
nificant reductions in the risk of death
from any cause and of death from
cardiovascular causes (10). The baseline
blood pressure among the study sub-
jects was 145/81 mmHg. Compared
with the placebo group, the patients
treated with a single-pill, fixed-dose
combination of perindopril and indapa-
mide experienced an average reduction
of 5.6 mmHg in SBP and 2.2 mmHg in
DBP. The final blood pressure in the
treated group was 136/73 mmHg, not
quite the intensive or tight control
achieved in ACCORD. Recently published
6-year follow-up of the ADVANCE-BP
study reported that the reductions in
the risk of death from any cause and of
death from cardiovascular causes in the
intervention group were attenuated, but
remained significant (11).
These results underscore the impor-
tant clinical difference between patients
who are able to easily achieve lower
blood pressure levels (e.g., as seen in
observational epidemiology studies)
and patients who require intensive
medical management to achieve these
goals (e.g., the clinical trials).
Systolic Blood Pressure
The clear body of evidence that SBP .140
mmHg is harmful suggests that clinicians
should promptly initiate and titrate ther-
apy in an ongoing fashion to achieve and
maintain SBP ,140 mmHg in virtually all
patients. Patients with long life expectancy
may have renal benefits from long-term
intensive blood pressure control. Addi-
tionally, individuals in whom stroke risk
is a concern may, as part of shared deci-
sion making, have appropriately lower sys-
tolic targets such as ,130 mmHg. This is
especially true if lower blood pressure can
be achieved with few drugs and without
side effects of therapy.
Diastolic Blood Pressure
Similarly, the clearest evidence from ran-
domized clinical trials supports DBP
targets of ,90 mmHg. Prior recommen-
dations for lower DBP targets (,80
mmHg) were based primarily on a post
hoc analysis of the Hypertension Optimal
Treatment (HOT) trial (12). This level may
still be appropriate for patients with long
life expectancy and those with chronic
kidney disease and elevated urine albu-
min excretion (12). The 2015 American
Diabetes Association (ADA) Standards of
Care have been revised to reflect the
higher-quality evidence that exists to
support a goal of DBP ,90 mmHg, al-
though lower targets may be appropriate
care.diabetesjournals.org
for certain individuals. This is in harmoni-
zation with a recent publication by the
Eighth Joint National Committee that rec-
ommended, for individuals over 18 years
of age with diabetes, a DBP threshold of
,90 mmHg and SBP ,140 mmHg (7).
Treatment Strategies
Lifestyle Modifications
Although there are no well-controlled
studies of diet and exercise in the treat-
ment of elevated blood pressure or hy-
pertension in individuals with diabetes,
the DASH study evaluated the impact of
healthy dietary patterns in individuals
without diabetes and has shown antihy-
pertensive effects similar to those of phar-
macological monotherapy.
Lifestyle therapy consists of restrict-
ing sodium intake (,2,300 mg/day); re-
ducing excess body weight; increasing
consumption of fruits, vegetables (8–
10 servings per day), and low-fat dairy
products (2–3 servings per day); avoid-
ing excessive alcohol consumption (no
more than 2 servings per day in men
and no more than 1 serving per day in
women) (13); and increasing activity lev-
els (14). For individuals with diabetes
and hypertension, setting a sodium in-
take goal of ,1,500 mg/day should be
considered on an individual basis.
These lifestyle (nonpharmacological)
strategies may also positively affect gly-
cemia and lipid control and should be
encouraged in those with even mildly
elevated blood pressure. The effects of
lifestyle therapy on cardiovascular
events have not been established. Non-
pharmacological therapy is reasonable
in individuals with diabetes and mildly
elevated blood pressure (SBP .120
mmHg or DBP .80 mmHg). If the blood
pressure is confirmed to be $140 mmHg
systolic and/or $90 mmHg diastolic,
pharmacological therapy should be ini-
tiated along with nonpharmacological
therapy (14). To enable long-term
adherence, lifestyle therapy should
be adapted to suit the needs of the pa-
tient and discussed as part of diabetes
management.
Pharmacological Interventions
Lowering of blood pressure with regi-
mens based on a variety of antihyper-
tensive agents, including ACE inhibitors,
ARBs, b-blockers, diuretics, and calcium
channel blockers, has been shown to be
effective in reducing cardiovascular
events. Several studies have suggested
that ACE inhibitors may be superior to
dihydropyridine calcium channel blockers
in reducing cardiovascular events (15–17).
However, several studies have also
shown no specific advantage to ACE inhib-
itors as initial treatment of hypertension
in the general hypertensive population,
while showing an advantage of initial
therapy with low-dose thiazide diuretics
on cardiovascular outcomes (14,18,19).
In people with diabetes, inhibitors of
the renin-angiotensin system (RAS) may
have unique advantages for initial or
early treatment of hypertension. In a tri-
al of individuals at high risk for CVD,
including a large subset with diabetes,
an ACE inhibitor reduced CVD outcomes
(20). In patients with congestive heart
failure (CHF), including subgroups with
diabetes, ARBs have been shown to re-
duce major CVD outcomes (21–24). In
type 2 diabetic patients with significant
diabetic kidney disease, ARBs were su-
perior to calcium channel blockers for
reducing heart failure (25). Although ev-
idence for distinct advantages of RAS
inhibitors on CVD outcomes in diabetes
remains conflicting (10,19), the high
CVD risks associated with diabetes, and
the high prevalence of undiagnosed
CVD, may still favor recommendations
for their use as first-line hypertension
therapy in people with diabetes (14).
The blood pressure arm of the
ADVANCE trial demonstrated that rou-
tine administration of a fixed combina-
tion of the ACE inhibitor perindopril and
the diuretic indapamide significantly re-
duced combined microvascular and
macrovascular outcomes, as well as death
from cardiovascular causes and total
mortality. The improved outcomes could
also have been due to lower achieved
blood pressure in the perindopril-
indapamide arm (10). Another trial
showed a decrease in morbidity and mor-
tality in those receiving benazepril and
amlodipine versus benazepril and hydro-
chlorothiazide (HCTZ). The compelling
benefits of RAS inhibitors in diabetic pa-
tients with albuminuria or renal insuffi-
ciency provide additional rationale for
these agents (see Section 9. Microvascu-
lar Complications and Foot Care). If
needed to achieve blood pressure targets,
amlodipine, HCTZ, or chlorthalidone can
be added. If eGFR is ,30 mL/min/m2, a
loop diuretic, rather than HCTZ or chlor-
thalidone, should be prescribed. Titration
of and/or addition of further blood
Position Statement S51
pressure medications should be made in
timely fashion to overcome clinical inertia
in achieving blood pressure targets.
Growing evidence suggests that there is
an association between increase in sleep-
time blood pressure and incidence of CVD
events. A randomized controlled trial of
448 participants with type 2 diabetes and
hypertension demonstrated reduced
cardiovascular events and mortality with
median follow-up of 5.4 years if at least
one antihypertensive medication was
given at bedtime (26). Consider adminis-
tering one or more antihypertensive med-
ications at bedtime (27).
An important caveat is that most pa-
tients with hypertension require multiple-
drug therapy to reach treatment goals (13).
Identifying and addressing barriers to
medication adherence (such as cost and
side effects) should routinely be done. If
blood pressure remains uncontrolled de-
spite confirmed adherence to optimal
doses of at least three antihypertensive
agents of different classifications, one of
which should be a diuretic, clinicians should
consider an evaluation for secondary forms
of hypertension.
Pregnancy and Antihypertensive
Medications
In a pregnancy complicated by diabetes
and chronic hypertension, target blood
pressure goals of SBP 110–129 mmHg
and DBP 65–79 mmHg are reasonable, as
they contribute to improved long-term
maternal health. Lower blood pressure
levels may be associated with im-
paired fetal growth. During pregnancy,
treatment with ACE inhibitors and ARBs
is contraindicated, since they may cause
fetal damage. Antihypertensive drugs
known to be effective and safe in preg-
nancy include methyldopa, labetalol, dil-
tiazem, clonidine, and prazosin. Chronic
diuretic use during pregnancy has been
associated with restricted maternal
plasma volume, which may reduce
uteroplacental perfusion (28).
DYSLIPIDEMIA/LIPID
MANAGEMENT
Recommendations
Screening
c In adults, a screening lipid profile is
reasonable at the time of first diag-
nosis, at the initial medical evalua-
tion, and/or at age 40 years and
periodically (e.g., every 1–2 years)
thereafter. E
S52 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015

patients in larger trials (31–35) and trials

Treatment Recommendations and
Goals
c Lifestyle modification focusing on
the reduction of saturated fat, trans
fat, and cholesterol intake; increase
of omega-3 fatty acids, viscous fiber,
and plant stanols/sterols; weight
loss (if indicated); and increased
physical activity should be recom-
mended to improve the lipid profile
in patients with diabetes. A
c Intensify lifestyle therapy and opti-
mize glycemic control for patients
with elevated triglyceride levels
($150 mg/dL [1.7 mmol/L]) and/or
low HDL cholesterol (,40 mg/dL
[1.0 mmol/L] for men, ,50 mg/dL
[1.3 mmol/L] for women). C For
patients with fasting triglyceride
levels $500 mg/dL (5.7 mmol/L),
evaluate for secondary causes
and consider medical therapy to
reduce risk of pancreatitis. C
c For patients of all ages with diabe-
tes and overt CVD, high-intensity
statin therapy should be added to
lifestyle therapy. A
c For patients with diabetes aged
,40 years with additional CVD risk
factors, consider using moderate-
or high-intensity statin and lifestyle
therapy. C
c For patients with diabetes aged
40–75 years without additional
CVD risk factors, consider using
moderate-intensity statin and life-
style therapy. A
c For patients with diabetes aged 40–
75 years with additional CVD risk fac-
tors, consider using high-intensity
statin and lifestyle therapy. B
c For patients with diabetes aged
.75 years without additional
CVD risk factors, consider using
moderate-intensity statin therapy
and lifestyle therapy. B
c For patients with diabetes aged .75
years with additional CVD risk fac-
tors, consider using moderate- or
high-intensity statin therapy and life-
style therapy. B
c In clinical practice, providers may
need to adjust intensity of statin
therapy based on individual patient
response to medication (e.g., side
effects, tolerability, LDL cholesterol
levels). E
c Cholesterol laboratory testing
may be helpful in monitoring
adherence to therapy, but may
not be needed once the patient
is stable on therapy. E
c Combination therapy (statin/
fibrate and statin/niacin) has not
been shown to provide additional
cardiovascular benefit above statin
therapy alone and is not generally
recommended. A
c Statin therapy is contraindicated
in pregnancy. B
Lifestyle Intervention
Lifestyle intervention, including MNT, in-
creased physical activity, weight loss, and
smoking cessation, may allow some pa-
tients to reduce CVD risk factors, such as
by lowering LDL cholesterol. Nutrition in-
tervention should be tailored according to
each patient’s age, diabetes type, pharma-
cological treatment, lipid levels, and medi-
cal conditions. Recommendations should
focus on reducing saturated fat, choles-
terol, and trans unsaturated fat intake
and increasing omega-3 fatty acids and vis-
cous fiber (such as in oats, legumes, and
citrus). Glycemic control can also benefi-
cially modify plasma lipid levels, particularly
in patients with very high triglycerides and
poor glycemic control.
Statin Treatment
Initiating Statin Therapy Based on Risk
Patients with type 2 diabetes have an
increased prevalence of lipid abnormal-
ities, contributing to their high risk of
CVD. Multiple clinical trials have demon-
strated significant effects of pharmaco-
logical (primarily statin) therapy on CVD
outcomes in individual subjects with
CHD and for primary CVD prevention
(29,30). Subgroup analyses of diabetic
Table 8.1—Recommendations for statin treatment in people with diabetes
Recommended
Age Risk factors statin dose*
,40 years None None
CVD risk factor(s)** Moderate or high
Overt CVD*** High
40–75 years None Moderate
CVD risk factors High
Overt CVD High
.75 years None Moderate
CVD risk factors Moderate or high
Overt CVD High
*In addition to lifestyle therapy.
**CVD risk factors include LDL cholesterol $100 mg/dL (2.6 mmol/L), high blood pressure,
smoking, and overweight and obesity.
***Overt CVD includes those with previous cardiovascular events or acute coronary syndromes.
in patients with diabetes (36,37)
showed significant primary and second-
ary prevention of CVD events 1/2 CHD
deaths in patients with diabetes. Meta-
analyses, including data from over
18,000 patients with diabetes from 14
randomized trials of statin therapy
(mean follow-up 4.3 years), demonstrate
a 9% proportional reduction in all-cause
mortality and 13% reduction in vascular
mortality, for each mmol/L reduction in
LDL cholesterol (38). As in those without
diabetes, absolute reductions in objective
CVD outcomes (CHD death and nonfatal
MI) are greatest in people with high base-
line CVD risk (known CVD and/or very high
LDL cholesterol levels), but the overall ben-
efits of statin therapy in people with diabe-
tes at moderate or high risk for CVD are
convincing (39,40). Statins are the drugs of
choice for LDL cholesterol lowering and car-
dioprotection.
Most trials of statins and CVD out-
comes tested specific doses of statins
against placebo or other statins, rather
than aiming for specific LDL cholesterol
goals (41). In light of this fact, the 2015
ADA Standards of Care have been revised
to recommend when to initiate and inten-
sify statin therapy (high versus moderate)
based on risk profile (Table 8.1).
The American College of Cardiology/
American Heart Association new Pooled
Cohort Equation, the “Risk Calculator,”
may be a useful tool to estimate 10-
year atherosclerotic CVD (http://my
.americanheart.org). Since diabetes it-
self confers increased risk for CVD, the
Risk Calculator has limited use for as-
sessing risk in individuals with diabetes.
The following recommendations are
Monitoring with lipid panel
Annually or as needed to monitor
for adherence
As needed to monitor adherence
As needed to monitor adherence
care.diabetesjournals.org
supported by evidence from trials focus-
ing specifically on patients with diabetes.
Age ‡40 Years
In all patients with diabetes aged $40
years, and if clinically indicated, moderate-
intensity statin treatment should be
considered, in addition to lifestyle ther-
apy. Clinical trials in high-risk patients,
such as those with acute coronary syn-
dromes or previous cardiovascular
events (42–44), have demonstrated
that more aggressive therapy with high
doses of statins led to a significant re-
duction in further events. Therefore, in
patients with increased cardiovascular
risk (e.g., LDL cholesterol $100 mg/dL
[2.6 mmol/L], high blood pressure, smok-
ing, and overweight/obesity) or with overt
CVD, high-dose statins are recommended.
For adults with diabetes over 75 years of
age, there are limited data regarding statin
therapy. Statin therapy should be individ-
ualized based on risk profile. High-dose
statins, if well tolerated, may still be appro-
priate and are recommended for older
adults with overt CVD. However, the risk-
benefit profile should be routinely evalu-
ated in this population, with downward
titration (e.g., high to moderate intensity)
performed as needed. See Section 10.
Older Adults for more details on clinical
considerations for this unique population.
Age <40 Years and/or Type 1 Diabetes
Very little clinical trial evidence exists
for type 2 diabetic patients under the
age of 40 years or for type 1 diabetic
patients of any age. In the Heart Protec-
tion Study (lower age limit 40 years), the
subgroup of ;600 patients with type 1
diabetes had a proportionately similar,
although not statistically significant, re-
duction in risk to patients with type 2
diabetes (32). Even though the data
are not definitive, similar statin treat-
ment approaches should be considered
for both type 1 and type 2 diabetic pa-
tients, particularly in the presence of
cardiovascular risk factors. Please refer
to “Type 1 Diabetes Mellitus and Cardio-
vascular Disease: A Scientific Statement
From the American Heart Association
and American Diabetes Association”
(45) for additional discussion.
Treatment with a moderate dose of sta-
tin should be considered if the patient has
increased cardiovascular risk (e.g., cardio-
vascular risk factors such as LDL cholesterol
$100 mg/dL) and with a high dose of statin
if the patient has overt CVD.
Ongoing Therapy and Monitoring
With Lipid Panel
In adults with diabetes, a screening lipid
profile (total cholesterol, LDL cholesterol,
HDL cholesterol, and triglycerides) is rea-
sonable at the time of first diagnosis, at
the initial medical evaluation, and/or at
age 40 and periodically (e.g., every 1–2
years) thereafter. Once a patient is on a
statin, testing for LDL cholesterol may be
considered on an individual basis to, for
example, monitor adherence and efficacy.
In cases where patients are adherent, but
LDL cholesterol level is not responding, clin-
ical judgment is recommended to deter-
mine the need for and timing of lipid panels.
In individual patients, the highly variable
LDL cholesterol–lowering response seen
with statins is poorly understood (46). Re-
duction of CVD events with statins corre-
lates very closely with LDL cholesterol
lowering (29). Clinicians should attempt to
find a dose or alternative statin that is tol-
erable, if side effects occur. There is evi-
dence for significant LDL cholesterol
lowering from even extremely low, less
than daily, statin doses (47).
When maximally tolerated doses of sta-
tins fail to significantly lower LDL choles-
terol (,30% reduction from the patient’s
baseline), there is no strong evidence that
combination therapy should be used to
achieve additional LDL cholesterol lower-
ing. Although niacin, fenofibrate, ezeti-
mibe, and bile acid sequestrants all offer
additional LDL cholesterol lowering to sta-
tins alone, there is insufficient evidence
that such combination therapy provides a
significant increment in CVD risk reduction
over statin therapy alone.
Treatment of Other Lipoprotein
Fractions or Targets
Hypertriglyceridemia should be addressed
with dietary and lifestyle changes. Severe
hypertriglyceridemia (.1,000 mg/dL) may
warrant immediate pharmacological ther-
apy (fibric acid derivatives or fish oil) to
reduce the risk of acute pancreatitis. If se-
vere hypertriglyceridemia is absent, then
therapy targeting HDL cholesterol or triglyc-
erides lacks the strong evidence base of
statin therapy. If HDL cholesterol is ,40
mg/dL and LDL cholesterol is between
100 and 129 mg/dL, a fibrate or niacin
might be used, especially if a patient is
intolerant to statins.
Low levels of HDL cholesterol, often as-
sociated with elevated triglyceride levels,
are the most prevalent pattern of dyslipi-
demia in persons with type 2 diabetes.
Position Statement S53
However, the evidence base for drugs
that target these lipid fractions is signifi-
cantly less robust than that for statin ther-
apy (48). In a large trial specific to diabetic
patients, fenofibrate failed to reduce over-
all cardiovascular outcomes (49).
Combination Therapy
Statin and Fibrate
Combination therapy (statin and fibrate)
may be efficacious for treatment for LDL
cholesterol, HDL cholesterol, and triglycer-
ides, but this combination is associated
with an increased risk for abnormal trans-
aminase levels, myositis, or rhabdomyoly-
sis. The risk of rhabdomyolysis is more
common with higher doses of statins and
with renal insufficiency and seems to be
lower when statins are combined with fe-
nofibrate than gemfibrozil (50).
In the ACCORD study, in patients with
type 2 diabetes who were at high risk for
CVD, the combination of fenofibrate and
simvastatin did not reduce the rate of fatal
cardiovascular events, nonfatal MI, or non-
fatal stroke, as compared with simvastatin
alone. Prespecified subgroup analyses sug-
gested heterogeneity in treatment effects
according to sex, with a benefit of combi-
nation therapy for men and possible harm
for women, and a possible benefit for pa-
tients with both triglyceride level $204
mg/dL (2.3 mmol/L) and HDL cholesterol
level #34 mg/dL (0.9 mmol/L) (51).
Statin and Niacin
The Atherothrombosis Intervention in Met-
abolic Syndrome With Low HDL/High Triglyc-
erides: Impact on Global Health Outcomes
(AIM-HIGH) trial randomized over 3,000 pa-
tients (about one-third with diabetes) with
established CVD, low LDL cholesterol levels
(,180 mg/dL [4.7 mmol/L]), low HDL cho-
lesterol levels (men ,40 mg/dL [1.0 mmol/L]
and women ,50 mg/dL [1.3 mmol/L]),
and triglyceride levels of 150–400 mg/dL
(1.7–4.5 mmol/L) to statin therapy plus
extended-release niacin or matching pla-
cebo. The trial was halted early due to
lack of efficacy on the primary CVD out-
come (first event of the composite of death
from CHD, nonfatal MI, ischemic stroke,
hospitalization for an acute coronary syn-
drome, or symptom-driven coronary or ce-
rebral revascularization) and a possible
increase in ischemic stroke in those on
combination therapy (52). Hence, combi-
nation therapy with niacin is not recom-
mended given the lack of efficacy on
major CVD outcomes, possible increase in
risk of ischemic stroke, and side effects.
S54 Position Statement
Diabetes With Statin Use
There is an increased risk of incident dia-
betes with statin use (53,54), which may
be limited to those with diabetes risk fac-
tors. These patients may benefit from di-
abetes screening when on statin therapy.
An analysis of one of the initial studies
suggested that statins were linked to di-
abetes risk, the cardiovascular event rate
reduction with statins far outweighed the
risk of incident diabetes even for patients
at highest risk for diabetes (55). The abso-
lute risk increase was small (over 5 years of
follow-up, 1.2% of participants on placebo
developed diabetes and 1.5% on rosuvas-
tatin) (56). A meta-analysis of 13 random-
ized statin trials with 91,140 participants
showed an odds ratio of 1.09 for a new
diagnosis of diabetes, so that (on average)
treatment of 255 patients with statins for
4 years resulted in one additional case of
diabetes, while simultaneously prevent-
ing 5.4 vascular events among those 255
patients (54). The RR-benefit ratio favor-
ing statins is further supported by meta-
analysis of individual data of over 170,000
persons from 27 randomized trials. This
demonstrated that individuals at low risk
of vascular disease, including those un-
dergoing primary prevention, received
benefits from statins that included reduc-
tions in major vascular events and vascu-
lar death without increase in incidence of
cancer or deaths from other causes (30).
ANTIPLATELET AGENTS
Recommendations
c Consider aspirin therapy (75–162
mg/day) as a primary prevention
strategy in those with type 1 or
type 2 diabetes at increased car-
diovascular risk (10-year risk
.10%). This includes most men
aged .50 years or women aged
.60 years who have at least one
additional major risk factor (family
history of CVD, hypertension,
smoking, dyslipidemia, or albu-
minuria). C
c Aspirin should not be recom-
mended for CVD prevention for
adults with diabetes at low CVD
risk (10-year CVD risk ,5%, such
as in men aged ,50 years and
women aged ,60 years with no
major additional CVD risk factors),
since the potential adverse effects
from bleeding likely offset the
potential benefits. C
Diabetes Care Volume 38, Supplement 1, January 2015
c In patients in these age-groups
with multiple other risk factors
(e.g., 10-year risk 5–10%), clinical
judgment is required. E
c Use aspirin therapy (75–162 mg/day)
as a secondary prevention strategy
in those with diabetes and a his-
tory of CVD. A
c For patients with CVD and docu-
mented aspirin allergy, clopidogrel
(75 mg/day) should be used. B
c Dual antiplatelet therapy is rea-
sonable for up to a year after an
acute coronary syndrome. B
Risk Reduction
Aspirin has been shown to be effective in
reducing cardiovascular morbidity and
mortality in high-risk patients with previ-
ous MI or stroke (secondary prevention).
Its net benefit in primary prevention
among patients with no previous cardio-
vascular events is more controversial,
both for patients with and without a his-
tory of diabetes (57,58). Two randomized
controlled trials of aspirin specifically in
patients with diabetes failed to show a
significant reduction in CVD end points,
raising questions about the efficacy of as-
pirin for primary prevention in people
with diabetes (59,60).
The Antithrombotic Trialists’ (ATT) col-
laborators published an individual patient-
level meta-analysis of the six large trials of
aspirin for primary prevention in the gen-
eral population. These trials collectively
enrolled over 95,000 participants, includ-
ing almost 4,000 with diabetes. Overall,
they found that aspirin reduced the risk
of vascular events by 12% (RR 0.88 [95%
CI 0.82–0.94]). The largest reduction was
for nonfatal MI with little effect on CHD
death (RR 0.95 [95% CI 0.78–1.15]) or total
stroke. There was some evidence of a dif-
ference in aspirin effect by sex: aspirin
significantly reduced CVD events in men,
but not in women. Conversely, aspirin had
no effect on stroke in men but significantly
reduced stroke in women. Sex differences
in aspirin’s effects have not been observed
in studies of secondary prevention (57). In
the six trials examined by the ATT collab-
orators, the effects of aspirin on major
vascular events were similar for patients
with or without diabetes: RR 0.88 (95% CI
0.67–1.15) and RR 0.87 (95% CI 0.79–
0.96), respectively. The confidence inter-
val was wider for those with diabetes
because of smaller numbers.
Aspirin appears to have a modest ef-
fect on ischemic vascular events with
the absolute decrease in events depend-
ing on the underlying CVD risk. The main
adverse effects appear to be an in-
creased risk of gastrointestinal bleeding.
The excess risk may be as high as 1–5 per
1,000 per year in real-world settings. In
adults with CVD risk greater than 1% per
year, the number of CVD events pre-
vented will be similar to or greater
than the number of episodes of bleeding
induced, although these complications
do not have equal effects on long-term
health (61).
Treatment Considerations
In 2010, a position statement of the ADA,
the American Heart Association, and the
American College of Cardiology Founda-
tion recommended that low-dose (75–162
mg/day) aspirin for primary prevention is
reasonable for adults with diabetes and
no previous history of vascular disease
who are at increased CVD risk (10-year
risk of CVD events over 10%) and who
are not at increased risk for bleeding.
This generally includes most men over
age 50 years and women over age 60
years who also have one or more of the
following major risk factors: smoking, hy-
pertension, dyslipidemia, family history of
premature CVD, and albuminuria (62).
However, aspirin is no longer recom-
mended for those at low CVD risk
(women under age 60 years and men
under age 50 years with no major CVD
risk factors; 10-year CVD risk under 5%)
as the low benefit is likely to be out-
weighed by the risks of significant bleed-
ing. Clinical judgment should be used for
those at intermediate risk (younger pa-
tients with one or more risk factors or
older patients with no risk factors; those
with 10-year CVD risk of 5–10%) until
further research is available. Aspirin
use in patients under the age of 21 years
is contraindicated due to the associated
risk of Reye syndrome.
Average daily dosages used in most
clinical trials involving patients with di-
abetes ranged from 50 to 650 mg but
were mostly in the range of 100 to
325 mg/day. There is little evidence to
support any specific dose, but using the
lowest possible dose may help reduce
side effects (63). In the U.S., the most
common low dose tablet is 81 mg.
Although platelets from patients with
diabetes have altered function, it is
care.diabetesjournals.org
unclear what, if any, impact that finding
has on the required dose of aspirin for
cardioprotective effects in the patient
with diabetes. Many alternate pathways
for platelet activation exist that are in-
dependent of thromboxane A2 and thus
not sensitive to the effects of aspirin
(64). Therefore, while “aspirin resis-
tance” appears higher in patients with
diabetes when measured by a variety of
ex vivo and in vitro methods (platelet
aggregometry, measurement of throm-
boxane B2), these observations alone
are insufficient to empirically recom-
mend that higher doses of aspirin be
used in this group at this time.
A P2Y12 receptor antagonist in com-
bination with aspirin should be used for
at least 1 year in patients following an
acute coronary syndrome. Evidence
supports use of either ticagrelor or clo-
pidogrel if no percutaneous coronary
intervention (PCI) was performed and
the use of clopidogrel, ticagrelor, or
prasugrel if PCI was performed (65).
CORONARY HEART DISEASE
Recommendations
Screening
c In asymptomatic patients, routine
screening for coronary artery dis-
ease (CAD) is not recommended
because it does not improve out-
comes as long as CVD risk factors
are treated. A
Treatment
c In patients with known CVD, use
aspirin and statin therapy (if not
contraindicated) A and consider
ACE inhibitor therapy C to reduce
the risk of cardiovascular events.
c In patients with a prior MI, b-blockers
should be continued for at least 2
years after the event. B
c In patients with symptomatic
heart failure, thiazolidinedione
treatment should not be used. A
c In patients with stable CHF, met-
formin may be used if renal func-
tion is normal but should be
avoided in unstable or hospital-
ized patients with CHF. B
In all patients with diabetes, cardio-
vascular risk factors should be assessed
at least annually. These risk factors
include dyslipidemia, hypertension,
smoking, a family history of premature
coronary disease, and the presence of
albuminuria. Abnormal risk factors
should be treated as described else-
where in these guidelines.
Screening
Candidates for advanced or invasive car-
diac testing include those with 1) typical
or atypical cardiac symptoms and 2) an
abnormal resting ECG. The screening of
asymptomatic patients with high CVD
risk is not recommended (39), in part
because these high-risk patients should
already be receiving intensive medical
therapy, an approach that provides sim-
ilar benefit as invasive revascularization
(66,67). There is also some evidence
that silent MI may reverse over time,
adding to the controversy concerning
aggressive screening strategies (68). A
randomized observational trial demon-
strated no clinical benefit to routine
screening of asymptomatic patients
with type 2 diabetes and normal ECGs
(69). Despite abnormal myocardial per-
fusion imaging in more than one in five
patients, cardiac outcomes were essen-
tially equal (and very low) in screened
versus unscreened patients. Accord-
ingly, indiscriminate screening is not
considered cost-effective. Studies have
found that a risk factor–based approach
to the initial diagnostic evaluation and
subsequent follow-up for CAD fails to
identify which patients with type 2 di-
abetes will have silent ischemia on
screening tests (70,71). Any benefit of
newer noninvasive CAD screening meth-
ods, such as computed tomography and
computed tomography angiography, to
identify patient subgroups for different
treatment strategies, remain unproven.
Although asymptomatic diabetic pa-
tients with higher coronary disease bur-
den have more future cardiac events
(72–74), the role of these tests beyond
risk stratification is not clear. Their rou-
tine use leads to radiation exposure and
may result in unnecessary invasive test-
ing such as coronary angiography and
revascularization procedures. The ulti-
mate balance of benefit, cost, and risks
of such an approach in asymptomatic
patients remains controversial, particu-
larly in the modern setting of aggressive
CVD risk factor control.
Lifestyle and Pharmacological
Interventions
Intensive lifestyle intervention focusing
on weight loss through decreased
Position Statement S55
caloric intake and increased physical ac-
tivity as performed in the Action for
Health in Diabetes (Look AHEAD) trial
may be considered for improving glu-
cose control, fitness, and some CVD
risk factors. Patients at increased CVD
risk should receive aspirin and a statin,
and ACE inhibitor or ARB therapy if hy-
pertensive, unless there are contraindi-
cations to a particular drug class. While
clear benefit exists for ACE inhibitor and
ARB therapy in patients with nephropa-
thy or hypertension, the benefits in pa-
tients with CVD in the absence of these
conditions are less clear, especially
when LDL cholesterol is concomitantly
controlled (75,76). In patients with a
prior MI, b-blockers should be contin-
ued for at least 2 years after the event
(77). A systematic review of 34,000 pa-
tients showed that metformin is as safe
as other glucose-lowering treatments in
patients with diabetes and CHF, even in
those with reduced left ventricular ejec-
tion fraction or concomitant chronic
kidney disease; however, metformin
should be avoided in hospitalized
patients (78).
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S56 Position Statement
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 S58 Diabetes Care Volume 38, Supplement 1, January 2015

American Diabetes Association

9. Microvascular Complications
and Foot Care
Diabetes Care 2015;38(Suppl. 1):S58–S66 | DOI: 10.2337/dc15-S012

NEPHROPATHY
Recommendations
c Optimize glucose control to reduce the risk or slow the progression of diabetic
kidney disease. A
c Optimize blood pressure control to reduce the risk or slow the progression of
diabetic kidney disease. A
Screening
POSITION STATEMENT

c At least once a year, quantitatively assess urinary albumin (e.g., urine albumin-
to-creatinine ratio [UACR]) and estimated glomerular filtration rate (eGFR) in
patients with type 1 diabetes duration of $5 years and in all patients with type
2 diabetes. B
Treatment
c An ACE inhibitor or angiotensin receptor blocker (ARB) is not recommended
for the primary prevention of diabetic kidney disease in patients with diabetes
who have normal blood pressure and normal UACR (,30 mg/g). B
c Either an ACE inhibitor or ARB is suggested for the treatment of the non-
pregnant patient with modestly elevated urinary albumin excretion (30–299
mg/day) C and is recommended for those with urinary albumin excretion
.300 mg/day. A
c When ACE inhibitors, ARBs, or diuretics are used, monitor serum creatinine
and potassium levels for the development of increased creatinine or changes
in potassium. E
c Continued monitoring of UACR in patients with albuminuria is reasonable to
assess progression of diabetic kidney disease. E
c When eGFR is ,60 mL/min/1.73 m2, evaluate and manage potential compli-
cations of chronic kidney disease (CKD). E
c Consider referral to a physician experienced in the care of kidney disease when
there is uncertainty about the etiology of kidney disease, difficult manage-
ment issues, or advanced kidney disease. B
Nutrition
c For people with diabetic kidney disease, reducing the amount of dietary pro-
tein below the recommended daily allowance of 0.8 g/kg/day (based on ideal
body weight) is not recommended because it does not alter glycemic mea-
sures, cardiovascular risk measures, or the course of GFR decline. A

The terms “microalbuminuria” (30–299 mg/24 h) and “macroalbuminuria”

(.300 mg/24 h) will no longer be used, since albuminuria occurs on a continuum.
Albuminuria is defined as UACR $30 mg/g.
Diabetic kidney disease occurs in 20–40% of patients with diabetes and is the
leading cause of end-stage renal disease (ESRD). Persistent increased albumin-
uria in the range of UACR 30–299 mg/g is an early indicator of diabetic kidney
disease in type 1 diabetes and a marker for development of diabetic kidney
disease in type 2 diabetes. It is a well-established marker of increased cardiovas-
cular disease (CVD) risk (1–3). However, there is increasing evidence of sponta-
neous remission of UACR levels 30–299 mg/g in up to 40% of patients with type 1
diabetes. About 30–40% remain with UACR levels of 30–299 mg/g and do not
Suggested citation: American Diabetes Association.
Microvascular complications and foot care. Sec. 9.
In Standards of Medical Care in Diabetesd2015.
Diabetes Care 2015;38(Suppl. 1):S58–S66
© 2015 by the American Diabetes Association.
Readers may use this article as long as the work
is properly cited, the use is educational and not
for profit, and the work is not altered.
care.diabetesjournals.org
progress to higher levels ($300 mg/g)
over 5–10 years of follow-up (4–7). Pa-
tients with persistent albuminuria are
likely to develop ESRD (8,9).
Interventions
Glycemia
A number of interventions have been
demonstrated to reduce the risk and
slow the progression of diabetic kid-
ney disease. Intensive diabetes man-
agement with the goal of achieving
near-normoglycemia has been shown
in large prospective randomized stud-
ies to delay the onset and progression
of increased urinary albumin excre-
tion and reduced eGFR in patients
with type 1 (9) and type 2 diabetes
(10–14).
Despite prior concerns and published
case reports, current data indicate that
the overall risk of metformin-associated
lactic acidosis is low (14). GFR may be a
more appropriate measure to assess
continued metformin use than serum
creatinine considering that the serum
creatinine level can translate into
widely varying eGFR levels depending
on age, ethnicity, and muscle mass
(15). A recent review (16) proposes
that metformin use should be reeval-
uated at an eGFR ,45 mL/min/1.73 m2
with a reduction in maximum dose to
1,000 mg/day and discontinued when
eGFR ,30 mL/min/1.73 m2 or in clini-
cal situations in which there is an in-
creased risk of lactic acidosis, such as
sepsis, hypotension, and hypoxia, or in
which there is a high risk of acute kid-
ney injury resulting in a worsening
of GFR, such as administration of
radiocontrast dye in those with eGFR
,60 mL/min/1.73 m2.
Blood Pressure
The UK Prospective Diabetes Study
(UKPDS) provided strong evidence that
blood pressure control can reduce the
development of diabetic kidney disease
(17). In addition, large prospective ran-
domized studies in patients with type 1
diabetes have shown that ACE inhibitors
have achieved lower systolic blood pres-
sure levels (,140 mmHg) and have
provided a selective benefit over other
antihypertensive drug classes in delay-
ing the progression of increased urinary
albumin excretion and can slow the de-
cline in GFR in patients with higher lev-
els of albuminuria (18,19). In patients
with type 2 diabetes, hypertension,
and normoalbuminuria, renin-angiotensin
system inhibition has been demon-
strated to delay onset of elevated al-
buminuria (20,21). Of note, in the
latter study, there was an unexpected
higher rate of fatal cardiovascular
events with olmesartan compared
with placebo among patients with pre-
existing CVD.
ACE inhibitors have been shown to
reduce major CVD outcomes (i.e.,
myocardial infarction, stroke, death)
in patients with diabetes (22), thus
further supporting the use of these
agents in patients with elevated
albuminuria, a CVD risk factor. ARBs
do not have the same beneficial effect
on cardiovascular outcomes or pre-
vent the onset of elevated albuminuria
in normotensive patients with type 1
or type 2 diabetes (23). However, ARBs
have been shown to reduce the pro-
gression of albuminuria, as well as
ESRD, in patients with type 2 diabetes
(24–26). In those with diabetic kidney
disease, some evidence suggests that
ARBs are associated with a smaller in-
crease in serum potassium levels com-
pared with ACE inhibitors (27).
Combination Therapy
Drug combinations that block the renin-
angiotensin system (e.g., an ACE inhibi-
tor plus an ARB, a mineralocorticoid
antagonist, or a direct renin inhibitor)
provide additional lowering of albumin-
uria (28). However, compared with
single-agent use, such combinations
have been found to provide no addi-
tional benefit on CVD or diabetic kid-
ney disease and have higher adverse
event rates (hyperkalemia or acute kid-
ney injury) (29). Therefore, the com-
bined use of different inhibitors of the
renin-angiotensin system should be
avoided.
Diuretics, calcium channel blockers,
and b-blockers can be used as additional
therapy to further lower blood pressure
in patients already treated with maxi-
mum doses of ACE inhibitors or ARBs
(30) or as alternate therapy in the rare
individual unable to tolerate ACE inhib-
itors and ARBs.
Studies in patients with varying
stages of diabetic kidney disease
have shown that the limitation of di-
etary protein to avoid excess intake
slows the progression of albuminuria,
GFR decline, and occurrence of ESRD
Position Statement S59
(31–34), although more recent studies
have provided conflicting results (35).
Dietary protein limitation, if protein
intake is high, is a consideration par-
ticularly in patients whose diabetic
kidney disease is progressing despite
optimal glucose and blood pressure
control and use of an ACE inhibitor or
ARB (34).
Assessment of Albuminuria Status and
Renal Function
Screening for increased urinary albu-
min excretion can be performed by
UACR in a random spot urine collec-
tion; 24-h or timed collections are
more burdensome and add little to
prediction or accuracy (36,37). Mea-
surement of a spot urine sample for
albumin alone (whether by immunoas-
say or by using a sensitive dipstick test
specific for albuminuria) without si-
multaneously measuring urine creati-
nine is less expensive but susceptible to
false-negative and false-positive deter-
minations as a result of variation in
urine concentration due to hydration
and other factors.
Abnormalities of albumin excretion
and the linkage between UACR and
24-h albumin excretion are defined in
Table 9.1. Because of variability in urinary
albumin excretion, two of three speci-
mens collected within a 3- to 6-month
period should be abnormal before
considering a patient to have developed
albuminuria. Exercise within 24 h, infec-
tion, fever, congestive heart failure,
marked hyperglycemia, and marked hy-
pertension may elevate urinary albumin
excretion over baseline values.
Abnormal urine albumin excretion
and GFR level may be used to stage
CKD. The National Kidney Foundation
classification (Table 9.2) is primarily
based on GFR levels and may be super-
seded by other systems in which staging
Table 9.1—Definitions of abnormalities
in albumin excretion
Spot collection
Category (mg/g creatinine)
Normal ,30
Increased urinary
albumin excretion* $30
*Historically, ratios between 30 and 299
mg/g have been called “microalbuminuria”
and those .300 mg/g have been called
“macroalbuminuria” (or clinical
albuminuria).
S60 Position Statement
includes other variables such as urinary
albumin excretion (38). Studies have
found decreased GFR without increased
urine albumin excretion in a substantial
percentage of adults with type 2 diabe-
tes (39). Substantial evidence shows
that in patients with type 1 diabetes
and persistent UACR 30–299 mg/g,
screening with albumin excretion rate
alone would miss .20% of progressive
disease (7). Serum creatinine with eGFR
should therefore be assessed at least
annually in all adults with diabetes, re-
gardless of the degree of urine albumin
excretion.
Serum creatinine should be used to
estimate GFR and to stage the level
of CKD, if present. eGFR is commonly
coreported by laboratories or can be
estimated using formulae such as the
Modification of Diet in Renal Disease
(MDRD) study equation (40) or the
Chronic Kidney Disease Epidemiology
Collaboration (CKD-EPI) equation. The
latter is the current preferred GFR es-
timating equation. GFR calculators are
available at http://www.nkdep.nih
.gov.
The need for annual quantitative as-
sessment of albumin excretion after
diagnosis of albuminuria and institu-
tion of ACE inhibitor or ARB therapy
and blood pressure control is a subject
of debate. Continued surveillance can
assess both response to therapy and
disease progression and may aid in as-
sessing adherence to ACE inhibitor or
ARB therapy. Some suggest that reduc-
ing UACR to normal (,30 mg/g) or
near normal may improve CKD and
CVD prognosis, but this approach has
not been formally evaluated in pro-
spective trials, and evidence demon-
strates spontaneous remission of
albuminuria in up to 40% of type 1 di-
abetic patients.
Conversely, patients with increasing
albumin levels, declining GFR, increas-
ing blood pressure, retinopathy, macro-
vascular disease, elevated lipids and/or
uric acid concentrations, or a family his-
tory of CKD are more likely to ex-
perience a progression of diabetic
kidney disease (7).
Complications of kidney disease cor-
relate with level of kidney function.
When the eGFR is ,60 mL/min/1.73 m2,
screening for complications of CKD
is indicated (Table 9.3). Early vacci-
nation against hepatitis B virus is
Diabetes Care Volume 38, Supplement 1, January 2015
Table 9.2—Stages of CKD
Stage Description GFR (mL/min/1.73 m2)
1 Kidney damage* with normal or increased GFR $90
2 Kidney damage* with mildly decreased GFR 60–89
3 Moderately decreased GFR 30–59
4 Severely decreased GFR 15–29
5 Kidney failure ,15 or dialysis
*Kidney damage is defined as abnormalities on pathological, urine, blood, or imaging tests.
Adapted from Levey et al. (37).
indicated in patients likely to progress treatment of blood pressure and blood
to ESRD. glucose, and the potential need for renal
transplant.
Referral to Nephrologist
Consider referral to a physician experi-
enced in the care of kidney disease RETINOPATHY
when there is uncertainty about the
Recommendations
etiology of kidney disease (heavy pro-
teinuria, active urine sediment, absence c Optimize glycemic control to re-
of retinopathy, rapid decline in GFR). duce the risk or slow the progres-
Other triggers for referral may include sion of retinopathy. A
difficult management issues (anemia, c Optimize blood pressure control
secondary hyperparathyroidism, meta- to reduce the risk or slow the pro-
bolic bone disease, resistant hyperten- gression of retinopathy. A
sion, or electrolyte disturbance) or
Screening
advanced kidney disease. The threshold
c Adults with type 1 diabetes
for referral may vary depending on
should have an initial dilated and
the frequency with which a provider
comprehensive eye examination
encounters diabetic patients with sig-
by an ophthalmologist or optom-
nificant kidney disease. Consultation
etrist within 5 years after the on-
with a nephrologist when stage 4 CKD
set of diabetes. B
develops has been found to reduce cost,
c Patients with type 2 diabetes
improve quality of care, and delay dial-
should have an initial dilated and
ysis (41). However, other specialists and
comprehensive eye examination
providers should not delay educating
by an ophthalmologist or optom-
their patients about the progressive na-
etrist shortly after the diagnosis of
ture of diabetic kidney disease, the kid-
diabetes. B
ney preservation benefits of proactive
Table 9.3—Management of CKD in diabetes (7)
GFR (mL/min/1.73 m2) Recommended management
All patients Yearly measurement of creatinine, urinary albumin excretion, potassium
45–60 Referral to a nephrologist if possibility for nondiabetic kidney
disease exists (duration of type 1 diabetes ,10 years, persistent
albuminuria, abnormal findings on renal ultrasound, resistant
hypertension, rapid fall in GFR, or active urinary sediment on
ultrasound)
Consider the need for dose adjustment of medications
Monitor eGFR every 6 months
Monitor electrolytes, bicarbonate, hemoglobin, calcium,
phosphorus, parathyroid hormone at least yearly
Assure vitamin D sufficiency
Consider bone density testing
Referral for dietary counseling
30–44 Monitor eGFR every 3 months
Monitor electrolytes, bicarbonate, calcium, phosphorus, parathyroid
hormone, hemoglobin, albumin, weight every 3–6 months
Consider the need for dose adjustment of medications
,30 Referral to a nephrologist
care.diabetesjournals.org Position Statement S61

Diabetic retinopathy is a highly specific in a population with well-controlled

c If there is no evidence of retinopathy
vascular complication of both type 1 type 2 diabetes, there was essentially
for one or more eye exams, then ex-
and type 2 diabetes, with prevalence no risk of development of significant ret-
ams every 2 years may be consid-
strongly related to the duration of dia- inopathy with a 3-year interval after a
ered. If diabetic retinopathy is
betes. Diabetic retinopathy is the most normal examination (49). Examinations
present, subsequent examinations
frequent cause of new cases of blind- will be required more frequently if reti-
for patients with type 1 and type 2
ness among adults aged 20–74 years. nopathy is progressing.
diabetes should be repeated annually
Glaucoma, cataracts, and other disor- Retinal photography, with remote
by an ophthalmologist or optome-
ders of the eye occur earlier and more reading by experts, has great potential
trist. If retinopathy is progressing or
frequently in people with diabetes. in areas where qualified eye care profes-
sight-threatening, then examinations
In addition to diabetes duration, fac- sionals are not readily available (50). It
will be required more frequently. B
tors that increase the risk of, or are as- also may enhance efficiency and reduce
c High-quality fundus photographs
sociated with, retinopathy include costs when the expertise of ophthalmol-
can detect most clinically signifi-
chronic hyperglycemia (42), nephropa- ogists can be used for more complex
cant diabetic retinopathy. Inter-
thy (43), and hypertension (44). Inten- examinations and for therapy (51). In-
pretation of the images should
sive diabetes management with the person exams are still necessary when
be performed by a trained eye
goal of achieving near-normoglycemia the photos are unacceptable and for
care provider. While retinal pho-
has been shown in large prospective follow-up if abnormalities are detected.
tography may serve as a screening
randomized studies to prevent and/or Photos are not a substitute for a com-
tool for retinopathy, it is not a sub-
delay the onset and progression of di- prehensive eye exam, which should be
stitute for a comprehensive eye
abetic retinopathy (11,45). Lowering performed at least initially and at inter-
exam, which should be performed
blood pressure has been shown to de- vals thereafter as recommended by an
at least initially and at intervals
crease retinopathy progression, al- eye care professional. Results of eye ex-
thereafter as recommended by
though tight targets (systolic ,120 aminations should be documented and
an eye care professional. E
mmHg) do not impart additional benefit transmitted to the referring health care
c Women with preexisting diabetes
(45). Several case series and a con- professional.
who are planning pregnancy or
trolled prospective study suggest that
who have become pregnant
pregnancy in type 1 diabetic patients Treatment
should have a comprehensive eye
may aggravate retinopathy (46,47). La- One of the main motivations for screening
examination and be counseled on
ser photocoagulation surgery can mini- for diabetic retinopathy is the long-
the risk of development and/or
mize this risk (47). established efficacy of laser photocoag-
progression of diabetic retinopa-
ulation surgery in preventing visual loss.
thy. Eye examination should occur
Screening Two large trials, the Diabetic Retinopa-
in the first trimester with close
The preventive effects of therapy and thy Study (DRS) in patients with PDR and
follow-up throughout pregnancy
the fact that patients with PDR or mac- the Early Treatment Diabetic Retinopathy
and for 1 year postpartum. B
ular edema may be asymptomatic pro- Study (ETDRS) in patients with macular
vide strong support for a screening edema, provide the strongest support
Treatment
program to detect diabetic retinopathy. for the therapeutic benefits of photoco-
c Promptly refer patients with any
Because retinopathy is estimated to agulation surgery. The DRS (52) showed
level of macular edema, severe
take at least 5 years to develop after that panretinal photocoagulation surgery
nonproliferative diabetic retinop-
the onset of hyperglycemia, patients reduced the risk of severe vision loss from
athy (NPDR), or any proliferative
with type 1 diabetes should have an ini- PDR from 15.9% in untreated eyes to
diabetic retinopathy (PDR) to an
tial dilated and comprehensive eye ex- 6.4% in treated eyes, with the greatest
ophthalmologist who is knowl-
amination within 5 years after the risk-benefit ratio in those with baseline
edgeable and experienced in the
diabetes diagnosis (48). Patients with disease (disc neovascularization or vitre-
management and treatment of di-
type 2 diabetes who may have had years ous hemorrhage).
abetic retinopathy. A
of undiagnosed diabetes and have a sig- The ETDRS (53) established the ben-
c Laser photocoagulation therapy is
nificant risk of prevalent diabetic ret- efit of focal laser photocoagulation sur-
indicated to reduce the risk of vision
inopathy at the time of diagnosis gery in eyes with macular edema,
loss in patients with high-risk PDR,
should have an initial dilated and com- particularly those with clinically signif-
clinically significant macular edema,
prehensive eye examination shortly af- icant macular edema, with reduction of
and, in some cases, severe NPDR. A
ter diagnosis. Examinations should be doubling of the visual angle (e.g., 20/50
c Antivascular endothelial growth
performed by an ophthalmologist or op- to 20/100) from 20% in untreated eyes
factor (VEGF) therapy is indicated
tometrist who is knowledgeable and to 8% in treated eyes. The ETDRS also
for diabetic macular edema. A
experienced in diagnosing diabetic reti- verified the benefits of panretinal pho-
c The presence of retinopathy is
nopathy. Subsequent examinations for tocoagulation for high-risk PDR and in
not a contraindication to aspirin
type 1 and type 2 diabetic patients are older-onset patients with severe NPDR
therapy for cardioprotection, as
generally repeated annually. Exams ev- or less-than-high-risk PDR.
aspirin does not increase the risk
ery 2 years may be cost-effective after Laser photocoagulation surgery in
of retinal hemorrhage. A
one or more normal eye exams, and both trials was beneficial in reducing
S62 Position Statement
the risk of further visual loss, but gener-
ally not beneficial in reversing already
diminished acuity. Recombinant mono-
clonal neutralizing antibody to VEGF im-
proves vision and reduces the need for
laser photocoagulation in patients with
macular edema (54). Other emerging
therapies for retinopathy include sus-
tained intravitreal delivery of fluocin-
olone (55) and the possibility of
prevention with fenofibrate (56,57).
NEUROPATHY
Recommendations
c All patients should be screened for
diabetic peripheral neuropathy
(DPN) starting at diagnosis of
type 2 diabetes and 5 years after
the diagnosis of type 1 diabetes
and at least annually thereafter,
using simple clinical tests, such
as a 10-g monofilament. B
c Screening for signs and symptoms
(e.g., orthostasis, resting tachycar-
dia) of cardiovascular autonomic
neuropathy (CAN) should be consid-
ered with more advanced disease. E
c Tight glycemic control is the only
strategy convincingly shown to
prevent or delay the development
of DPN and CAN in patients with
type 1 diabetes A and to slow the
progression of neuropathy in some
patients with type 2 diabetes. B
c Assess and treat patients to re-
duce pain related to DPN B and
symptoms of autonomic neuropa-
thy and to improve quality of life. E
The diabetic neuropathies are heteroge-
neous with diverse clinical manifestations.
They may be focal or diffuse. The most
prevalent neuropathies are DPN and auto-
nomic neuropathy. Although DPN is a diag-
nosis of exclusion, complex investigations
or referral for neurology consultation to ex-
clude other conditions is rarely needed.
The early recognition and appropriate
management of neuropathy in the pa-
tient with diabetes is important for a
number of reasons:
1. Nondiabetic neuropathies may be
present in patients with diabetes
and may be treatable.
2. A number of treatment options exist
for symptomatic diabetic neuropathy.
3. Up to 50% of DPN may be asymptom-
atic, and patients are at risk for in-
sensate injury to their feet.
Diabetes Care Volume 38, Supplement 1, January 2015
4. Autonomic neuropathy, particularly
CAN, is an independent risk factor
for cardiovascular mortality (58,59).
Specific treatment for the underlying
nerve damage, other than improved gly-
cemic control, is currently not available.
Glycemic control was shown to effec-
tively prevent DPN and CAN in type 1
diabetes (60,61) and may modestly
slow progression in type 2 diabetes
(13) but does not reverse neuronal
loss. Therapeutic strategies (pharmaco-
logical and nonpharmacological) for the
relief of specific symptoms related to
painful DPN or autonomic neuropathy
are recommended because they can po-
tentially reduce pain (62) and improve
quality of life.
Diagnosis
Diabetic Peripheral Neuropathy
Patients with diabetes should be
screened annually for DPN symptoms
using simple clinical tests. Symptoms
vary according to the class of sensory
fibers involved. The most common
symptoms are induced by the involve-
ment of small fibers and include pain,
dysesthesias (unpleasant abnormal sen-
sations of burning and tingling), and
numbness. Clinical tests include assess-
ment of pinprick sensation, vibration
threshold using a 128-Hz tuning fork,
light touch perception using a 10-g
monofilament, and ankle reflexes. As-
sessment should follow the typical
DPN pattern, starting distally (the dorsal
aspect of the hallux) on both sides and
move proximally until threshold is de-
tected. Several clinical instruments
that combine more than one test have
.87% sensitivity in detecting DPN
(63–65). Electrophysiological testing or
referral to a neurologist is rarely needed,
except in situations where the clinical
features are atypical or the diagnosis is
unclear.
In patients with severe or atypical neu-
ropathy, causes other than diabetes
should always be considered, such as neu-
rotoxic medications, heavy metal poison-
ing, alcohol abuse, vitamin B12 deficiency
(66), renal disease, chronic inflammatory
demyelinating neuropathy, inherited neu-
ropathies, and vasculitis (67).
Diabetic Autonomic Neuropathy
The symptoms and signs of autonomic
dysfunction should be elicited care-
fully during the history and physical
examination. Major clinical manifesta-
tions of diabetic autonomic neuropathy
include resting tachycardia, exercise
intolerance, orthostatic hypotension,
gastroparesis, constipation, erectile dys-
function, sudomotor dysfunction, im-
paired neurovascular function, and,
potentially, autonomic failure in response
to hypoglycemia.
Cardiovascular Autonomic Neuropathy
CAN is the most studied and clinically
important form of diabetic autonomic
neuropathy because of its association
with mortality independent of other
cardiovascular risk factors (58,68). In
early stages, CAN may be completely
asymptomatic and detected by changes
in heart rate variability with deep
breathing and abnormal cardiovascular
reflex tests (R-R interval response to
deep breathing, standing, and Valsalva
maneuver tests). Advanced disease may
be indicated by resting tachycardia
(.100 bpm) and orthostasis (a fall in
systolic blood pressure .20 mmHg or
diastolic blood pressure of at least 10
mmHg upon standing without an appro-
priate heart rate response). The stan-
dard cardiovascular reflex tests (deep
breathing, standing, and Valsalva
maneuver) are noninvasive, easy to
perform, reliable, and reproducible, es-
pecially the deep breathing test, and
have prognostic value (69). Although
some societies have developed guide-
lines for screening for CAN, the benefits
of sophisticated testing beyond risk
stratification are not clear (69).
Gastrointestinal Neuropathies
Gastrointestinal neuropathies (e.g.,
esophageal enteropathy, gastroparesis,
constipation, diarrhea, fecal inconti-
nence) may involve any section of the
gastrointestinal tract. Gastroparesis
should be suspected in individuals with
erratic glucose control or with upper gas-
trointestinal symptoms without another
identified cause. Evaluation of solid-
phase gastric emptying using double-
isotope scintigraphy may be done if
symptoms are suggestive, but test re-
sults often correlate poorly with symp-
toms. Constipation is the most common
lower-gastrointestinal symptom but can
alternate with episodes of diarrhea.
Genitourinary Tract Disturbances
Diabetic autonomic neuropathy is also
associated with genitourinary tract dis-
turbances. In men, diabetic autonomic
care.diabetesjournals.org
neuropathy may cause erectile dysfunc-
tion and/or retrograde ejaculation. Eval-
uation of bladder dysfunction should be
performed for individuals with diabetes
who have recurrent urinary tract infec-
tions, pyelonephritis, incontinence, or a
palpable bladder.
Treatment
Glycemic Control
Tight glycemic control, implemented
early in the course of diabetes, has
been shown to effectively prevent or de-
lay the development of DPN and CAN in
patients with type 1 diabetes (70–73).
While the evidence is not as strong for
type 2 diabetes, some studies have
demonstrated a modest slowing of pro-
gression (74,75) without reversal of
neuronal loss. Several observational
studies further suggest that neuropathic
symptoms improve not only with opti-
mization of glycemic control but also
with the avoidance of extreme blood
glucose fluctuations.
Diabetic Peripheral Neuropathy
DPN symptoms, and especially neuro-
pathic pain, can be severe, have sudden
onset, and are associated with lower
quality of life, limited mobility, depres-
sion, and social dysfunction (76). There
is limited clinical evidence regarding the
most effective treatments for individual
patients given the wide range of avail-
able medications (77,78). Several drugs
have been approved specifically for re-
lief of DPN pain in the U.S. (pregabalin,
duloxetine, and tapentadol), but none
affords complete relief, even when
used in combination. Venlafaxine, ami-
triptyline, gabapentin, valproate, and
other opioids (morphine sulfate, trama-
dol, oxycodone controlled release) may
be effective and may be considered for
treatment of painful DPN. Head-to-
head treatment comparisons and stud-
ies that include quality-of-life outcomes
are rare, so treatment decisions must
consider each patient’s presentation
and comorbidities and often follow a
trial-and-error approach. Given the
range of partially effective treatment
options, a tailored and stepwise phar-
macological strategy with careful atten-
tion to relative symptom improvement,
medication adherence, and medication
side effects is recommended to achieve
pain reduction and improve quality of
life (62).
Autonomic Neuropathy
An intensive multifactorial cardiovascu-
lar risk intervention targeting glucose,
blood pressure, lipids, smoking, and
other lifestyle factors has been shown
to reduce the progression and develop-
ment of CAN among patients with type 2
diabetes (79). For those with significant
CAN, referral to a cardiologist may be
indicated.
Orthostatic Hypotension
Treatment of orthostatic hypotension is
challenging. The therapeutic goal is to
minimize postural symptoms rather
than to restore normotension. Most pa-
tients require the use of both pharma-
cological and nonpharmacological
measures (e.g., avoiding medications
that aggravate hypotension, using com-
pressive garments over the legs and ab-
domen). Midodrine is the only drug
approved by the U.S. Food and Drug
Administration for the treatment of
orthostatic hypotension.
Gastroparesis Symptoms
Gastroparesis symptoms may improve
with dietary changes and prokinetic agents
such as erythromycin. Recently, the Euro-
pean Medicines Agency (www.ema.europa
.eu/docs/en_GB/document_library/
Press_release/2013/07/WC500146614.pdf)
decided that risks of extrapyramidal symp-
toms with metoclopramide outweigh ben-
efits. In Europe, metoclopramide use is
now restricted to a maximum of 5 days
and is no longer indicated for the long-
term treatment of gastroparesis. Although
the U.S. Food and Drug Administration’s
decision is pending, it is suggested that
metoclopramide be reserved for only the
most severe cases that are unresponsive
to other therapies. Side effects should be
closely monitored.
Erectile Dysfunction
Treatments for erectile dysfunction may
include phosphodiesterase type 5 inhibi-
tors, intracorporeal or intraurethral prosta-
glandins, vacuum devices, or penile
prostheses. Interventions for other mani-
festations of autonomic neuropathy are
described in the American Diabetes Asso-
ciation (ADA) statement on neuropathy
(78). As with DPN treatments, these inter-
ventions do not change the underlying
pathology and natural history of the dis-
ease process but may have a positive im-
pact on the quality of life of the patient.
Position Statement S63
FOOT CARE
Recommendations
c For all patients with diabetes, per-
form an annual comprehensive
foot examination to identify risk
factors predictive of ulcers and
amputations. The foot examina-
tion should include inspection
and assessment of foot pulses. B
c Patients with insensate feet, foot
deformities, and ulcers should
have their feet examined at every
visit. E
c Provide general foot self-care
education to all patients with di-
abetes. B
c A multidisciplinary approach is
recommended for individuals
with foot ulcers and high-risk feet
(e.g., dialysis patients and those
with Charcot foot, prior ulcers, or
amputation). B
c Refer patients who smoke or who
have a loss of protective sensation
(LOPS), structural abnormalities,
or a history of prior lower-
extremity complications to foot
care specialists for ongoing pre-
ventive care and lifelong surveil-
lance. C
c Initial screening for peripheral
arterial disease (PAD) should
include a history for claudication
and an assessment of the pedal
pulses. C
c Refer patients with significant
claudication or a positive ankle-
brachial index (ABI) for further
vascular assessment and consider
exercise, medications, and surgical
options. C
Amputation and foot ulceration, which
are consequences of diabetic neuropa-
thy and/or PAD, are common and repre-
sent major causes of morbidity and
disability in people with diabetes. Loss
of 10-g monofilament perception and
reduced vibration perception predict
foot ulcers (78). Early recognition and
management of risk factors can prevent
or delay adverse outcomes.
The risk of ulcers or amputations is
increased in people who have the fol-
lowing risk factors:
○ Previous amputation
○ Past foot ulcer history
○ Peripheral neuropathy
○ Foot deformities
S64 Position Statement
○ Peripheral vascular disease
○ Visual impairment
○ Diabetic nephropathy (especially pa-
tients on dialysis)
○ Poor glycemic control
○ Cigarette smoking
Clinicians are encouraged to review
ADA screening recommendations for
further details and practical descriptions
of how to perform components of the
comprehensive foot examination (80).
Examination
All adults with diabetes should
undergo a comprehensive foot exami-
nation at least annually to identify
high-risk conditions. Clinicians should
ask about history of previous foot ulcer-
ation or amputation, neuropathic or pe-
ripheral vascular symptoms, impaired
vision, tobacco use, and foot care prac-
tices. A general inspection of skin integ-
rity and musculoskeletal deformities
should be done in a well-lit room. Vas-
cular assessment would include inspec-
tion and assessment of pedal pulses.
The neurological exam recommended
is designed to identify LOPS rather than
early neuropathy. The clinical examination
to identify LOPS is simple and requires no
expensive equipment. Five simple clinical
tests (use of a 10-g monofilament, vibra-
tion testing using a 128-Hz tuning fork,
tests of pinprick sensation, ankle reflex as-
sessment, and testing vibration percep-
tion threshold with a biothesiometer),
each with evidence from well-conducted
prospective clinical cohort studies, are
considered useful in the diagnosis of
LOPS in the diabetic foot. Any of the five
tests listed above could be used by clini-
cians to identify LOPS, although ideally
two of these should be regularly per-
formed during the screening examd
normally the 10-g monofilament and one
other test. One or more abnormal tests
would suggest LOPS, while at least two
normal tests (and no abnormal test) would
rule out LOPS. The last test listed, vibration
assessment using a biothesiometer or sim-
ilar instrument, is widely used in the U.S.;
however, identification of the patient with
LOPS can easily be carried out without this
or other expensive equipment.
Screening
Initial screening for PAD should
include a history for claudication and
an assessment of the pedal pulses.
Diabetes Care Volume 38, Supplement 1, January 2015
A diagnostic ABI should be considered
in patients with PAD. Due to the high
estimated prevalence of PAD in patients
with diabetes and the fact that many
patients with PAD are asymptomatic,
an ADA consensus report on PAD (81)
suggested that a screening ABI be per-
formed in patients over 50 years of age
and be considered in patients under 50
years of age who have other PAD risk
factors (e.g., smoking, hypertension, hy-
perlipidemia, or duration of diabetes
.10 years). Refer patients with signifi-
cant symptoms or a positive ABI for fur-
ther vascular assessment and consider
exercise, medications, and surgical
options (81).
Patient Education
Patients with diabetes and high-risk foot
conditions should be educated about
their risk factors and appropriate man-
agement. Patients at risk should under-
stand the implications of LOPS; the
importance of foot monitoring on a daily
basis; the proper care of the foot, includ-
ing nail and skin care; and the selection
of appropriate footwear. Patients with
LOPS should be educated on ways to
substitute other sensory modalities
(hand palpation, visual inspection) for
surveillance of early foot problems. Pa-
tients’ understanding of these issues
and their physical ability to conduct
proper foot surveillance and care should
be assessed. Patients with visual difficul-
ties, physical constraints preventing
movement, or cognitive problems that
impair their ability to assess the condi-
tion of the foot and to institute appro-
priate responses will need other people,
such as family members, to assist in
their care.
Treatment
People with neuropathy or evidence of
increased plantar pressure (e.g., ery-
thema, warmth, callus, or measured
pressure) may be adequately managed
with well-fitted walking shoes or athletic
shoes that cushion the feet and redis-
tribute pressure. Calluses can be de-
brided with a scalpel by a foot care
specialist or other health professional
with experience and training in foot
care. People with bony deformities (e.g.,
hammertoes, prominent metatarsal
heads, bunions) may need extra wide
or deep shoes. People with extreme
bony deformities (e.g., Charcot foot)
who cannot be accommodated with
commercial therapeutic footwear may
need custom-molded shoes.
Most diabetic foot infections are poly-
microbial, with aerobic gram-positive
cocci (GPC). Staphylococci are the most
common causative organisms. Wounds
without evidence of soft-tissue or bone
infection do not require antibiotic ther-
apy. Empiric antibiotic therapy can be
narrowly targeted at GPC in many
acutely infected patients, but those at
risk for infection with antibiotic-resistant
organisms or with chronic, previously
treated, or severe infections require
broader-spectrum regimens and should
be referred to specialized care centers
(82). Foot ulcers and wound care may
require care by a podiatrist, orthopedic
or vascular surgeon, or rehabilitation
specialist experienced in the manage-
ment of individuals with diabetes.
Guidelines for treatment of diabetic
foot ulcers have recently been updated
(82).
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Diabetes Care Volume 38, Supplement 1, January 2015 S67

American Diabetes Association

10. Older Adults
Diabetes Care 2015;38(Suppl. 1):S67–S69 | DOI: 10.2337/dc15-S013

Recommendations
c Older adults who are functional and cognitively intact and have significant life
expectancy should receive diabetes care with goals similar to those developed
for younger adults. E
c Glycemic goals for some older adults might reasonably be relaxed, using in-
dividual criteria, but hyperglycemia leading to symptoms or risk of acute
hyperglycemic complications should be avoided in all patients. E
c Other cardiovascular risk factors should be treated in older adults with con-
sideration of the time frame of benefit and the individual patient. Treatment
of hypertension is indicated in virtually all older adults, and lipid-lowering and

POSITION STATEMENT
aspirin therapy may benefit those with life expectancy at least equal to the
time frame of primary or secondary prevention trials. E
c Screening for diabetes complications should be individualized in older adults,
but particular attention should be paid to complications that would lead to
functional impairment. E
c Older adults ($65 years of age) with diabetes should be considered a high-
priority population for depression screening and treatment. B

Diabetes is an important health condition for the aging population; at least 20% of
patients over the age of 65 years have diabetes, and this number is expected to grow
rapidly in the coming decades. Older individuals with diabetes have higher rates of
premature death, functional disability, and coexisting illnesses, such as hyperten-
sion, coronary heart disease, and stroke, than those without diabetes. Older adults
with diabetes are also at a greater risk than other older adults for several common
geriatric syndromes, such as polypharmacy, cognitive impairment, urinary inconti-
nence, injurious falls, and persistent pain. Screening for diabetes complications in
older adults also should be individualized. Older adults are at an increased risk for
depression and should therefore be screened and treated accordingly (1). Particular
attention should be paid to complications that can develop over short periods of
time and/or that would significantly impair functional status, such as visual and
lower-extremity complications. Please refer to the American Diabetes Association
consensus report “Diabetes in Older Adults” for details (2).
The care of older adults with diabetes is complicated by their clinical and func-
tional heterogeneity. Some older individuals developed diabetes years earlier and
may have significant complications; others are newly diagnosed and may have had
years of undiagnosed diabetes with resultant complications; and still other older
adults may have truly recent-onset disease with few or no complications. Some
older adults with diabetes are frail and have other underlying chronic conditions,
substantial diabetes-related comorbidity, or limited physical or cognitive functioning.
Other older individuals with diabetes have little comorbidity and are active.
Life expectancies are highly variable for this population but are often longer than
clinicians realize. Providers caring for older adults with diabetes must take this hetero-
geneity into consideration when setting and prioritizing treatment goals (Table 10.1).

Suggested citation: American Diabetes Associa-

TREATMENT GOALS tion. Older adults. Sec. 10. In Standards of Med-
ical Care in Diabetesd2015. Diabetes Care
There are few long-term studies in older adults demonstrating the benefits of in-
2015;38(Suppl. 1):S67–S69
tensive glycemic, blood pressure, and lipid control. Patients who can be expected to
© 2015 by the American Diabetes Association.
live long enough to reap the benefits of long-term intensive diabetes management, Readers may use this article as long as the work
who have good cognitive and physical function, and who choose to do so via shared is properly cited, the use is educational and not
decision making may be treated using therapeutic interventions and goals similar to for profit, and the work is not altered.
S68 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015

Table 10.1—Framework for considering treatment goals for glycemia, blood pressure, and dyslipidemia in older adults with
diabetes
Fasting or Bedtime Blood
Patient characteristics/ Reasonable preprandial glucose pressure
health status Rationale A1C goal‡ glucose (mg/dL) (mg/dL) (mmHg) Lipids
Healthy (few coexisting Longer remaining life ,7.5% 90–130 90–150 ,140/90 Statin unless
chronic illnesses, intact expectancy contraindicated
cognitive and functional or not tolerated
status)
Complex/intermediate Intermediate remaining ,8.0% 90–150 100–180 ,140/90 Statin unless
(multiple coexisting life expectancy, high contraindicated
chronic illnesses* or 21 treatment burden, or not tolerated
instrumental ADL hypoglycemia
impairments or mild-to- vulnerability, fall risk
moderate cognitive
impairment)
Very complex/poor health Limited remaining life ,8.5%† 100–180 110–200 ,150/90 Consider likelihood of
(long-term care or end- expectancy makes benefit with statin
stage chronic illnesses** benefit uncertain (secondary prevention
or moderate-to-severe more so than primary)
cognitive impairment or
21 ADL dependencies)
This represents a consensus framework for considering treatment goals for glycemia, blood pressure, and dyslipidemia in older adults with diabetes.
The patient characteristic categories are general concepts. Not every patient will clearly fall into a particular category. Consideration of patient and
caregiver preferences is an important aspect of treatment individualization. Additionally, a patient’s health status and preferences may change over
time. ADL, activities of daily living.
‡A lower A1C goal may be set for an individual if achievable without recurrent or severe hypoglycemia or undue treatment burden.
*Coexisting chronic illnesses are conditions serious enough to require medications or lifestyle management and may include arthritis, cancer,
congestive heart failure, depression, emphysema, falls, hypertension, incontinence, stage 3 or worse chronic kidney disease, myocardial infarction,
and stroke. By “multiple,” we mean at least three, but many patients may have five or more (6).
**The presence of a single end-stage chronic illness, such as stage 3–4 congestive heart failure or oxygen-dependent lung disease, chronic kidney
disease requiring dialysis, or uncontrolled metastatic cancer, may cause significant symptoms or impairment of functional status and significantly
reduce life expectancy.
†A1C of 8.5% equates to an estimated average glucose of ;200 mg/dL. Looser glycemic targets than this may expose patients to acute risks from
glycosuria, dehydration, hyperglycemic hyperosmolar syndrome, and poor wound healing.

those for younger adults with diabetes.
As with all diabetic patients, diabetes
self-management education and ongo-
ing diabetes self-management support
are vital components of diabetes care
for older adults and their caregivers.
For patients with advanced diabetes
complications, life-limiting comorbid ill-
ness, or substantial cognitive or func-
tional impairment, it is reasonable to
set less intensive glycemic target goals.
These patients are less likely to benefit
from reducing the risk of microvascular
complications and more likely to suffer
serious adverse effects from hypoglyce-
mia. However, patients with poorly con-
trolled diabetes may be subject to acute
complications of diabetes, including
dehydration, poor wound healing, and
hyperglycemic hyperosmolar coma.
Glycemic goals at a minimum should
avoid these consequences.
Although hyperglycemia control may
be important in older individuals with
diabetes, greater reductions in morbid-
ity and mortality are likely to result from
control of other cardiovascular risk
factors rather than from tight glycemic
control alone. There is strong evidence
from clinical trials of the value of treat-
ing hypertension in the elderly (3,4).
There is less evidence for lipid-lowering
and aspirin therapy, although the bene-
fits of these interventions for primary
and secondary prevention are likely to
apply to older adults whose life expec-
tancies equal or exceed the time frames
seen in clinical trials.
HYPOGLYCEMIA
Older adults are at a higher risk of hypo-
glycemia for many reasons, including in-
sulin deficiency and progressive renal
insufficiency. In addition, older adults
tend to have higher rates of unidentified
cognitive deficits, causing difficulty in
complex self-care activities (e.g., glucose
monitoring, adjusting insulin doses, etc.).
These deficits have been associated with
increased risk of hypoglycemia and with
severe hypoglycemia linked to increased
dementia. Therefore, it is important to
routinely screen older adults for cognitive
dysfunction and discuss findings with the
caregivers. Hypoglycemic events should
be diligently monitored, and glycemic tar-
gets may need to be adjusted to accom-
modate for the changing needs of the
older adult (2).
PHARMACOLOGICAL THERAPY
Special care is required in prescribing and
monitoring pharmacological therapy in
older adults. Cost may be a significant
factor, especially as older adults tend to
be on many medications. Metformin may
be contraindicated because of renal insuf-
ficiency or significant heart failure. Thia-
zolidinediones, if used at all, should be
used very cautiously in those with, or at
risk for, congestive heart failure and have
been associated with fractures. Sulfonyl-
ureas, other insulin secretagogues, and
insulin can cause hypoglycemia. Insulin
use requires that patients or caregivers
have good visual and motor skills and cog-
nitive ability. GLP-1 agonists and dipep-
tidyl peptidase-4 inhibitors have few
side effects, but their costs may be a bar-
rier to some older patients. A clinical trial,
Saxagliptin Assessment of Vascular
care.diabetesjournals.org
Outcomes Recorded in Patients with
Diabetes Mellitus–Thrombolysis in Myo-
cardial Infarction 53 (SAVOR-TIMI 53),
evaluated saxagliptin (a dipeptidyl
peptidase-4 inhibitor) and its impact
on cardiovascular outcomes (5). Pa-
tients treated with saxagliptin were
more likely to be hospitalized for heart
failure than were those given a placebo
(3.5% vs. 2.8%, respectively, according to
2-year Kaplan-Meier estimates; hazard
ratio 1.27 [95% CI 1.0721.51]; P 5 0.007).
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EO, Huang ES. Classification of older adults who
have diabetes by comorbid conditions, United
States, 2005-2006. Prev Chronic Dis 2012;9:E100
 S70 Diabetes Care Volume 38, Supplement 1, January 2015

American Diabetes Association

11. Children and Adolescents
Diabetes Care 2015;38(Suppl. 1):S70–S76 | DOI: 10.2337/dc15-S014

TYPE 1 DIABETES
Three-quarters of all cases of type 1 diabetes are diagnosed in individuals ,18 years of
age. The provider must consider the unique aspects of care and management of children
and adolescents with type 1 diabetes, such as changes in insulin sensitivity related to
sexual maturity and physical growth, ability to provide self-care, supervision in child care
and school, and unique neurological vulnerability to hypoglycemia and possibly hyper-
glycemia as well as diabetic ketoacidosis. Attention to family dynamics, developmental
stages, and physiological differences related to sexual maturity are all essential in de-
veloping and implementing an optimal diabetes regimen. Due to the paucity of clinical
research in children, the recommendations for children and adolescents are less likely to
POSITION STATEMENT

be based on clinical trial evidence. However, expert opinion and a review of available
and relevant experimental data are summarized in the American Diabetes Association
(ADA) position statement “Care of Children and Adolescents With Type 1 Diabetes” (1)
and have been updated in the recently published ADA position statement “Type 1
Diabetes Through the Life Span” (2).
A multidisciplinary team of specialists trained in pediatric diabetes management
and sensitive to the challenges of children and adolescents with type 1 diabetes should
provide care for this population. It is essential that diabetes self-management educa-
tion (DSME) and support (DSMS), medical nutrition therapy (MNT), and psychosocial
support be provided at diagnosis and regularly thereafter by individuals experienced
with the educational, nutritional, behavioral, and emotional needs of the growing
child and family. The balance between adult supervision and self-care should be de-
fined at the first interaction and reevaluated at each clinic visit. This relationship will
evolve as the child reaches physical, psychological, and emotional maturity.

Glycemic Control

Recommendation
c An A1C goal of ,7.5% is recommended across all pediatric age-groups. E

Current standards for diabetes management reflect the need to lower glucose as
safely as possible. This should be done with stepwise goals. Special consideration
should be given to the unique risks of hypoglycemia in young children (aged ,6
years), as they are often unable to recognize, articulate, and/or manage their hy-
poglycemic symptoms. This “hypoglycemia unawareness” should be considered
when establishing individualized glycemic targets.
Although it was previously thought that young children were at risk for cognitive
impairment after episodes of severe hypoglycemia, current data have not confirmed
this (3–5). Furthermore, new therapeutic modalities, such as rapid- and long-acting insulin
analogs, technological advances (e.g., continuous glucose monitors, low glucose suspend
insulin pumps), and education, may mitigate the incidence of severe hypoglycemia (6). The
Diabetes Control and Complications Trial (DCCT) demonstrated that near-normalization
of blood glucose levels was more difficult to achieve in adolescents than in adults.
Nevertheless, the increased use of basal–bolus regimens and insulin pumps in youth from
infancy through adolescence has been associated with more children reaching the blood Suggested citation: American Diabetes Associa-
glucose targets set by the ADA (7–9) in those families in which both parents and the child tion. Children and adolescents. Sec. 11. In Stan-
dards of Medical Care in Diabetesd2015.
with diabetes participate jointly to perform the required diabetes-related tasks. Further-
Diabetes Care 2015;38(Suppl. 1):S70–S76
more, studies documenting neurocognitive imaging differences related to hyperglycemia
© 2015 by the American Diabetes Association.
in children provide another compelling motivation for lowering glycemic targets (10). Readers may use this article as long as the work
In selecting glycemic goals, the long-term health benefits of achieving a lower A1C is properly cited, the use is educational and not
should be balanced against the risks of hypoglycemia and the developmental burdens for profit, and the work is not altered.
care.diabetesjournals.org Position Statement S71

of intensive regimens in children and

youth. In addition, achieving lower A1C
levels is more likely to be related to set-
ting lower A1C targets (11). A1C goals are
presented in Table 11.1.
Autoimmune Conditions
Recommendation
c Assess for the presence of addi-
tional autoimmune conditions at di-
agnosis and if symptoms develop. E
Because of the increased frequency of
other autoimmune diseases in type 1 di-
abetes, screening for thyroid dysfunc-
tion, vitamin B 12 deficiency (due to
autoimmune gastritis), and celiac dis-
ease should be considered based on
signs and symptoms. Periodic screening
in asymptomatic individuals has been
recommended, but the effectiveness
and optimal frequency are unclear.
Although less common than celiac
disease and thyroid dysfunction, there
are other autoimmune conditions that
occur more commonly in type 1 diabe-
tes, such as Addison’s disease (primary
adrenal insufficiency), autoimmune
hepatitis, dermatomyositis, myasthenia
gravis, etc., which should be assessed
and monitored as clinically indicated.
Celiac Disease
Recommendations
c Consider screening children with
type 1 diabetes for celiac disease
by measuring tissue transglutami-
nase or deamidated gliadin antibod-
ies, with documentation of normal
total serum IgA levels, soon after the
diagnosis of diabetes. E
c Consider screening in children with a
positive family history of celiac dis-
ease, growth failure, failure to gain
weight, weight loss, diarrhea, flatu-
lence, abdominal pain, or signs of
malabsorption or in children with
frequent unexplained hypoglycemia
or deterioration in glycemic control. E
c Children with biopsy-confirmed
celiac disease should be placed
on a gluten-free diet and have
consultation with a dietitian expe-
rienced in managing both diabetes
and celiac disease. B
Celiac disease is an immune-mediated
disorder that occurs with increased fre-
quency in patients with type 1 diabetes
(1–16% of individuals compared with 0.3–
1% in the general population) (12,13).
Testing for celiac disease includes mea-
suring serum levels of IgA antitissue
transglutaminase antibodies or, with IgA
deficiency, screening can include measur-
ing IgG tissue transglutaminase antibodies
or IgG deamidated gliadin peptide antibod-
ies. A small-bowel biopsy in antibody-
positive children is recommended to
confirm the diagnosis (14). European guide-
lines on screening for celiac disease in chil-
dren (not specific to children with type 1
diabetes) suggested that biopsy may not be
necessary in symptomatic children with
high-positive antibody titers as long as fur-
ther testing such as genetic or HLA testing
was supportive, but that asymptomatic at-
risk children should have biopsies (15).
In symptomatic children with type 1 di-
abetes and confirmed celiac disease,
gluten-free diets reduce symptoms and
rates of hypoglycemia (16). The challenging
dietary restrictions associated with having
both type 1 diabetes and celiac disease
place a significant burden on individuals.
Therefore, we recommend a biopsy con-
firming the diagnosis of celiac disease be-
fore endorsing significant dietary changes,
especially in asymptomatic children.
Thyroid Disease
Recommendations
c Consider testing children with
type 1 diabetes for antithyroid
peroxidase and antithyroglobulin
antibodies soon after diagnosis. E
c Measuring thyroid-stimulating hor-
mone concentrations soon after
diagnosis of type 1 diabetes is
reasonable. If normal, consider re-
checking every 1–2 years or sooner
if the patient develops symptoms
of thyroid dysfunction, thyrome-
galy, an abnormal growth rate, or
unusual glycemic variation. E
Autoimmune thyroid disease is the most
common autoimmune disorder associ-
ated with diabetes, occurring in 17–
30% of patients with type 1 diabetes
(17). About one-quarter of children
with type 1 diabetes have thyroid auto-
antibodies at the time of diagnosis (18),
and the presence of thyroid autoantibod-
ies is predictive of thyroid dysfunctiond
most commonly hypothyroidism, al-
though hyperthyroidism may occur (19).
Subclinical hypothyroidism may be asso-
ciated with increased risk of symptomatic
hypoglycemia (20) and reduced linear
growth. Hyperthyroidism alters glucose
metabolism, potentially resulting in dete-
rioration of metabolic control.
Management of Cardiovascular Risk
Factors
Hypertension
Recommendations
Screening
c Blood pressure should be mea-
sured at each routine visit. Chil-
dren found to have high-normal
blood pressure (systolic blood
pressure [SBP] or diastolic blood
pressure [DBP] $90th percentile
for age, sex, and height) or hyper-
tension (SBP or DBP $95th per-
centile for age, sex, and height)
should have blood pressure con-
firmed on three separate days. B

Table 11.1—Plasma blood glucose and A1C goals for type 1 diabetes across all pediatric age-groups
Plasma blood glucose goal range
Before meals Bedtime/overnight A1C Rationale
90–130 mg/dL 90–150 mg/dL ,7.5% A lower goal (,7.0%) is reasonable if it can be
(5.0–7.2 mmol/L) (5.0–8.3 mmol/L) achieved without excessive hypoglycemia
Key concepts in setting glycemic goals:
c Goals should be individualized, and lower goals may be reasonable based on benefit-risk assessment.
c Blood glucose goals should be modified in children with frequent hypoglycemia or hypoglycemia unawareness.
c Postprandial blood glucose values should be measured when there is a discrepancy between preprandial blood glucose values and A1C levels
and to help assess glycemia in those on basal–bolus regimens.
S72 Position Statement
Treatment
c Initial treatment of high-normal
blood pressure (SBP or DBP consis-
tently $90th percentile for age,
sex, and height) includes dietary
intervention and exercise, aimed
at weight control and increased
physical activity, if appropriate. If
target blood pressure is not
reached with 3–6 months of
lifestyle intervention, pharmaco-
logical treatment should be con-
sidered. E
c Pharmacological treatment of hy-
pertension (SBP or DBP consistently
$95th percentile for age, sex, and
height) should be considered as
soon as hypertension is confirmed. E
c ACE inhibitors or angiotensin recep-
tor blockers (ARBs) should be consid-
ered for the initial pharmacological
treatment of hypertension, following
appropriate reproductive counsel-
ing due to its potential teratogenic
effects. E
c The goal of treatment is blood
pressure consistently ,90th per-
centile for age, sex, and height. E
Blood pressure measurements should
be determined correctly, using the ap-
propriate size cuff, and with the child
seated and relaxed. Hypertension
should be confirmed on at least three
separate days. Evaluation should pro-
ceed as clinically indicated. Treatment
is generally initiated with an ACE inhibi-
tor, but an ARB can be used if the ACE
inhibitor is not tolerated (e.g., due to
cough). Normal blood pressure levels for
age, sex, and height and appropriate
methods for measurement are available
online at www.nhlbi.nih.gov/health/
prof/heart/hbp/hbp_ped.pdf.
Dyslipidemia
Recommendations
Testing
c Obtain a fasting lipid profile on
children $2 years of age soon af-
ter the diagnosis (after glucose
control has been established). E
c If lipids are abnormal, annual
monitoring is reasonable. If LDL
cholesterol values are within
the accepted risk levels (,100
mg/dL [2.6 mmol/L]), a lipid
profile repeated every 5 years is
reasonable. E
Diabetes Care Volume 38, Supplement 1, January 2015
Treatment
c Initial therapy may consist of opti-
mization of glucose control and
MNT using a Step 2 American Heart
Association (AHA) diet aimed at a
decrease in the amount of satu-
rated fat in the diet. B
c After the age of 10 years, the addi-
tion of a statin in patients who, after
MNT and lifestyle changes, have
LDL cholesterol .160 mg/dL (4.1
mmol/L) or LDL cholesterol .130
mg/dL (3.4 mmol/L) and one or
more cardiovascular disease (CVD)
risk factors is reasonable. E
c The goal of therapy is an LDL cho-
lesterol value ,100 mg/dL (2.6
mmol/L). E
Children diagnosed with type 1 diabetes
have a high risk of early subclinical (21,22)
and clinical (23) CVD. Although intervention
data are lacking, the AHA categorizes chil-
dren with type 1 diabetes in the highest tier
for cardiovascular risk and recommends
both lifestyle and pharmacological treat-
ment for those with elevated LDL choles-
terol levels (24,25). Initial therapy should be
with a Step 2 AHA diet, which restricts sat-
urated fat to 7% of total calories and re-
stricts dietary cholesterol to 200 mg/day.
Data from randomized clinical trials in chil-
dren as young as 7 months of age indicate
that this diet is safe and does not interfere
with normal growth and development (26).
For children with significant family his-
tory of CVD, the National Heart, Lung, and
Blood Institute recommends a fasting lipid
panel beginning at 2 years of age (27).
Abnormal results from a random lipid
panel should be confirmed with a fasting
lipid panel. Evidence has shown that im-
proved glucose control correlates with a
more favorable lipid profile. However, im-
proved glycemic control alone will not re-
verse significant dyslipidemia (28).
Neither long-term safety nor cardiovas-
cular outcome efficacy of statin therapy
has been established for children. How-
ever, studies have shown short-term
safety equivalent to that seen in adults
and efficacy in lowering LDL cholesterol
levels, improving endothelial function,
and causing regression of carotid intimal
thickening (29,30). Statins are not ap-
proved for use in patients under the age
of 10 years, and statin treatment should
generally not be used in children with
type 1 diabetes prior to this age. For post-
pubertal girls, issues of pregnancy
prevention are paramount, as statins
are category X in pregnancy (see Section
12. Management of Diabetes in Preg-
nancy for more information).
Smoking
Recommendation
c Elicit smoking history at initial and
follow-up diabetes visits and dis-
courage smoking in nonsmoking
youth and encourage smoking ces-
sation in those who smoke. B
The adverse health effects of smoking
are well recognized with respect to fu-
ture cancer and CVD risk. In youth with
diabetes, it remains important to avoid
additional CVD risk factors; thus, dis-
couraging cigarette smoking, including
e-cigarettes, is important as part of rou-
tine diabetes care. In younger children,
it is important to assess exposure to cig-
arette smoke in the home due to the
adverse effects of secondhand smoke
and to discourage youth from adopting
smoking behaviors if exposed to them in
childhood. In addition, smoking has
been associated with onset of albumin-
uria; therefore, avoiding smoking is im-
portant to prevent both microvascular
and macrovascular complications (31,32).
Microvascular Complications
Nephropathy
Recommendations
Screening
c At least an annual screening for
albuminuria, with a random spot
urine sample for albumin-to-
creatinine ratio (UACR), should
be considered once the child has
had diabetes for 5 years. B
c Measure creatinine clearance/es-
timated glomerular filtration rate
at initial evaluation and then
based on age, diabetes duration,
and treatment. E
Treatment
c Treatment with an ACE inhibitor,
titrated to normalization of albumin
excretion, should be considered
when elevated UACR (.30 mg/g)
is documented with at least two
of three urine samples. This should
be obtained over a 6-month inter-
val following efforts to improve
glycemic control and normalize
blood pressure for age. B
care.diabetesjournals.org
Recent research demonstrates the im-
portance of tight glycemic and blood
pressure control, especially as diabetes
duration increases (33). A creatinine
clearance using an estimated glomeru-
lar filtration rate can be obtained with
the serum creatinine, height, age, and
sex of the patient (34) and should be
obtained at baseline and repeated as in-
dicated based on clinical status, age, di-
abetes duration, and therapies. There
are ongoing clinical trials assessing the
efficacy of early treatment with ACE in-
hibitors for persistent albuminuria (35).
Retinopathy
Recommendations
c An initial dilated and comprehen-
sive eye examination should be
considered for the child at the
start of puberty or at age $10
years, whichever is earlier, once
the youth has had diabetes for 3–
5 years. B
c After the initial examination, an-
nual routine follow-up is generally
recommended. Less frequent ex-
aminations, every 2 years, may be
acceptable on the advice of an eye
care professional. E
Although retinopathy (like albuminuria)
most commonly occurs after the onset
of puberty and after 5–10 years of diabe-
tes duration (36), it has been reported in
prepubertal children and with diabetes
duration of only 1–2 years. Referrals
should be made to eye care professionals
with expertise in diabetic retinopathy, an
understanding of retinopathy risk in the
pediatric population, and experience in
counseling the pediatric patient and fam-
ily on the importance of early prevention/
intervention.
Neuropathy
Recommendation
c Consider an annual comprehen-
sive foot exam for the child at
the start of puberty or at age
$10 years, whichever is earlier,
once the youth has had type 1 di-
abetes for 5 years. E
Neuropathy rarely occurs in prepubertal
children or in youth with 1–2 years of
duration of diabetes (36). A comprehen-
sive foot exam, including inspection,
palpation of dorsalis pedis and posterior
tibial pulses, assessment of the pres-
ence or absence of patellar and Achilles
reflexes, and determination of proprio-
ception, vibration, and monofilament
sensation, should be performed annu-
ally along with assessment of symptoms
of neuropathic pain. Foot inspection can
be performed at each visit as education
for youth regarding the importance of
foot care.
Diabetes Self-management
Education and Support
Recommendation
c Youth with type 1 diabetes and
parents/caregivers (for patients
aged ,18 years) should receive
culturally sensitive and develop-
mentally appropriate individual-
ized DSME and DSMS according
to national standards when their
diabetes is diagnosed and rou-
tinely thereafter. B
No matter how sound the medical
regimen, it can only be as good as
the ability of the family and/or indi-
vidual to implement it. Family in-
volvement remains an important
component of optimal diabetes man-
agement throughout childhood and
adolescence. Health care providers
who care for children and adoles-
cents, therefore, must be capable of
evaluating the educational, behav-
ioral, emotional, and psychosocial fac-
tors that impact implementation of a
treatment plan and must work with
the individual and family to overcome
barriers or redefine goals as appropri-
ate. DSME and DSMS are activities
that require ongoing reassessment,
especially as the youth grows, devel-
ops, and acquires need for greater
self-care skills. In addition, it may be
necessary to assess the educational
needs and skills of day care providers,
school nurses, or school personnel who
may participate in the care of the young
child with diabetes (37).
School and Child Care
As a large portion of a child’s day is spent
in school, close communication with and
cooperation of school or day care per-
sonnel is essential for optimal diabetes
management, safety, and maximal aca-
demic opportunities. Please refer to the
ADA position statements “Diabetes Care
in the School and Day Care Setting” (38)
Position Statement S73
and “Care of Young Children With
Diabetes in the Child Care Setting” (39)
for additional details.
Transition From Pediatric to Adult
Care
Recommendations
c As teens transition into emerging
adulthood, health care providers
and families must recognize their
many vulnerabilities B and prepare
the developing teen, beginning in
early to mid-adolescence and at
least 1 year prior to the transition. E
c Both pediatricians and adult
health care providers should assist
in providing support and links to
resources for the teen and emerg-
ing adult. B
Care and close supervision of diabetes
management are increasingly shifted
from parents and other adults to the
youth with diabetes throughout child-
hood and adolescence. However, the
shift from pediatrics to adult health
care providers often occurs very abruptly
as the older teen enters the next devel-
opmental stage referred to as emerging
adulthood (40), which is a critical period
for young people who have diabetes.
During this period of major life transi-
tions, youth begin to move out of their
parents’ home and must become fully
responsible for their diabetes care. Their
new responsibilities include the many as-
pects of managing self-care, making
medical appointments, and financing
health care, once they are no longer cov-
ered under their parents’ health insur-
ance (although ongoing coverage until
age 26 years is possible with recent
U.S. health care reform). In addition to
lapses in health care, this is also a period
of deterioration in glycemic control; in-
creased occurrence of acute complica-
tions and psychosocial, emotional, and
behavioral issues; and emergence of
chronic complications (41–44).
Although scientific evidence contin-
ues to be limited, it is clear that compre-
hensive and coordinated planning,
beginning early and with ongoing atten-
tion, facilitates a seamless transition
from pediatric to adult health care
(41,42). Transition planning should be-
gin in early adolescence. Even after the
transition to adult care is made, support
and reinforcement are recommended.
S74 Position Statement
A comprehensive discussion regarding
the challenges faced during this period,
including specific recommendations, is
found in the ADA position statement “Di-
abetes Care for Emerging Adults: Recom-
mendations for Transition From Pediatric
to Adult Diabetes Care Systems” (42).
The National Diabetes Education
Program (NDEP) has materials avail-
able to facilitate the transition process
(http://ndep.nih.gov/transitions), and
the Endocrine Society in collaboration
with ADA and other organizations has
developed transition tools for clini-
cians and youth and families (http://
www.endo-society.org/clinicalpractice/
transition_of_care.cfm).
TYPE 2 DIABETES
For information on testing for type 2 di-
abetes and prediabetes in children and
adolescents, please refer to Section 2.
Classification and Diagnosis of Diabetes.
The Centers for Disease Control and
Prevention recently published projec-
tions for type 2 diabetes prevalence us-
ing the SEARCH database. Assuming a
2.3% annual increase, the prevalence
of type 2 diabetes in those under 20
years of age will quadruple in 40 years
(45,46). Given the current obesity epi-
demic, distinguishing between type 1
and type 2 diabetes in children can be
difficult. For example, autoantibodies
and ketosis may be present in patients
with features of type 2 diabetes (includ-
ing obesity and acanthosis nigricans).
Nevertheless, accurate diagnosis is crit-
ical as treatment regimens, educational
approaches, dietary counsel, and out-
comes will differ markedly between
the two diagnoses.
Significant comorbidities may already
be present at the time of a type 2 diabe-
tes diagnosis (47). It is recommended that
blood pressure measurement, a fasting
lipid panel, assessment for albumin excre-
tion, and dilated eye examination be
performed at diagnosis. Thereafter,
screening guidelines and treatment rec-
ommendations for hypertension, dyslipi-
demia, albumin excretion, and retinopathy
in youth with type 2 diabetes are similar to
those for youth with type 1 diabetes. Ad-
ditional problems that may need to be ad-
dressed include polycystic ovary disease
and the various comorbidities associated
with pediatric obesity, such as sleep
apnea, hepatic steatosis, orthopedic com-
plications, and psychosocial concerns. The
Diabetes Care Volume 38, Supplement 1, January 2015
ADA consensus report “Type 2 Diabetes in
Children and Adolescents” (48) provides
guidance on the prevention, screening,
and treatment of type 2 diabetes and its
comorbidities in young people.
PSYCHOSOCIAL ISSUES
Recommendations
c At diagnosis and during routine
follow-up care, assess psychoso-
cial issues and family stresses
that could impact adherence with
diabetes management and pro-
vide appropriate referrals to
trained mental health professionals,
preferably experienced in child-
hood diabetes. E
c Encourage developmentally ap-
propriate family involvement in di-
abetes management tasks for
children and adolescents, recog-
nizing that premature transfer of
diabetes care to the child can re-
sult in nonadherence and deterio-
ration in glycemic control. B
Diabetes management throughout
childhood and adolescence places sub-
stantial burdens on the youth and fam-
ily, necessitating ongoing assessment of
psychosocial issues and distress during
routine diabetes visits (49–51). Further,
the complexities of diabetes manage-
ment require ongoing parental involve-
ment in care throughout childhood with
developmentally appropriate family
teamwork between the growing child/
teen and parent in order to maintain
adherence and prevent deterioration
in glycemic control (52,53). In addition,
as diabetes-specific family conflict is re-
lated to poorer adherence and glycemic
control, it is appropriate to inquire
about such conflict during visits and to
either help negotiate a plan for resolu-
tion or refer to an appropriate mental
health specialist (54).
Screening for psychosocial distress
and mental health problems is an impor-
tant component of ongoing care. It is
important to consider the impact of di-
abetes on quality of life as well as the
development of mental health problems
related to diabetes distress, fear of hy-
poglycemia (and hyperglycemia), symp-
toms of anxiety, disordered eating
behaviors as well as eating disorders,
and symptoms of depression (55). Con-
sider screening for depression and
disordered eating behaviors using avail-
able screening tools, and, with respect
to disordered eating, it is important to
recognize the unique and dangerous
disordered eating behavior of insulin
omission for weight control in type 1
diabetes (49,56). The presence of a
mental health professional on pediatric
multidisciplinary teams highlights the
importance of attending to the psycho-
social issues of diabetes. These psycho-
social factors are significantly related to
nonadherence, suboptimal glycemic
control, reduced quality of life, and higher
rates of acute and chronic diabetes
complications.
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26. Salo P, Viikari J, Hämäläinen M, et al. Serum
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29. McCrindle BW, Ose L, Marais AD. Efficacy
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30. Wiegman A, Hutten BA, de Groot E, et al.
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the American Association of Clinical Endocrinol-
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the Centers for Disease Control and Prevention,
Children with Diabetes, The Endocrine Society,
the International Society for Pediatric and Ado-
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52. Katz ML, Volkening LK, Butler DA, Anderson
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53. Laffel LMB, Vangsness L, Connell A, Goebel-
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Demographic and clinical correlates of
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495–500
Diabetes Care Volume 38, Supplement 1, January 2015 S77

American Diabetes Association

12. Management of Diabetes in
Pregnancy
Diabetes Care 2015;38(Suppl. 1):S77–S79 | DOI: 10.2337/dc15-S015

For guidelines related to the diagnosis of gestational diabetes mellitus (GDM),

please refer to Section 2. Classification and Diagnosis of Diabetes.

Recommendations
c Provide preconception counseling that addresses the importance of tight
control in reducing the risk of congenital anomalies with an emphasis on
achieving A1C ,7%, if this can be achieved without hypoglycemia. B
c Potentially teratogenic medications (ACE inhibitors, statins, etc.) should be
avoided in sexually active women of childbearing age who are not using reli-

POSITION STATEMENT
able contraception. B
c GDM should be managed first with diet and exercise, and medications should
be added if needed. A
c Women with pregestational diabetes should have a baseline ophthalmology
exam in the first trimester and then be monitored every trimester as indicated
by degree of retinopathy. B
c Due to alterations in red blood cell turnover that lower the normal A1C level in
pregnancy, the A1C target in pregnancy is ,6% if this can be achieved without
significant hypoglycemia. B
c Medications widely used in pregnancy include insulin, metformin, and glybur-
ide; most oral agents cross the placenta or lack long-term safety data. B

DIABETES IN PREGNANCY
The prevalence of diabetes in pregnancy has been increasing in the U.S. The majority is
GDM with the remainder divided between pregestational type 1 diabetes and type 2
diabetes. Both pregestational type 1 diabetes and type 2 diabetes confer significantly
greater risk than GDM, with differences according to type as outlined below.

PRECONCEPTION COUNSELING
All women of childbearing age with diabetes should be counseled about the impor-
tance of strict glycemic control prior to conception. Observational studies show an
increased risk of diabetic embryopathy, especially anencephaly, microcephaly, and
congenital heart disease, that increases directly with elevations in A1C. Spontane-
ous abortion is also increased in the setting of uncontrolled diabetes. While obser-
vational studies are confounded by the relationship between elevated
periconceptional A1C and other poor self-care behaviors, the quantity and consistency
of data are convincing, and the recommendation remains to aim for an A1C ,7% prior
to conception to minimize risk (1,2). There are opportunities to educate adolescents of
reproductive age with diabetes about the risks of unplanned pregnancies and the
opportunities for healthy maternal and fetal outcomes with pregnancy planning (3).
Targeted preconception counseling visits should include routine rubella, rapid plasma
reagin, hepatitis B virus, and HIV testing as well as Pap smear, cervical cultures, blood
typing, and prescription of prenatal vitamins (with at least 400 mg of folic acid). Diabetes- Suggested citation: American Diabetes Asso-
specific management should include A1C, thyroid-stimulating hormone, creatinine, and ciation. Management of diabetes in preg-
urine albumin-to-creatinine ratio testing; review of the medication list for potentially nancy. Sec. 12. In Standards of Medical Care
in Diabetesd2015. Diabetes Care 2015;38
teratogenic drugs (i.e., ACE inhibitors, statins); and referral for an ophthalmologic exam.
(Suppl. 1):S77–S79
Specific risks of uncontrolled diabetes include fetal anomalies, preeclampsia,
© 2015 by the American Diabetes Association.
macrosomia, intrauterine fetal demise, neonatal hypoglycemia, and neonatal hy- Readers may use this article as long as the work
perbilirubinemia, among others. In addition, diabetes in pregnancy increases the is properly cited, the use is educational and not
risk of obesity and type 2 diabetes in offspring later in life (4,5). for profit, and the work is not altered.
S78 Position Statement
GLYCEMIC TARGETS IN
PREGNANCY
The goals for glycemic control for GDM
are based on recommendations from the
Fifth International Workshop-Conference
on Gestational Diabetes Mellitus (6) and
have the following targets for maternal
capillary glucose concentrations:
○ Preprandial #95 mg/dL (5.3 mmol/L)
and either
○ One-hour postmeal #140 mg/dL
(7.8 mmol/L) or
○ Two-hour postmeal #120 mg/dL
(6.7 mmol/L)
For women with preexisting type 1
diabetes or type 2 diabetes who be-
come pregnant, the following are rec-
ommended as optimal glycemic goals
if they can be achieved without exces-
sive hypoglycemia (7):
○ Premeal, bedtime, and overnight
glucose 60–99 mg/dL (3.3–5.4
mmol/L)
○ Peak postprandial glucose 100–129
mg/dL (5.4–7.1 mmol/L)
○ A1C ,6.0%
Metabolic physiology of pregnancy is
characterized by fasting hypoglycemia
due to insulin-independent glucose up-
take by the placenta, postprandial hyper-
glycemia, and carbohydrate intolerance
as a result of diabetogenic placental hor-
mones. In addition, insulin resistance in-
creases exponentially during the second
trimester and levels off toward the end of
the third trimester.
Reflecting this physiology, pre- and
postprandial monitoring of blood glucose
is recommended to achieve metabolic
control. The American College of
Obstetricians and Gynecologists (ACOG)
recommends the following targets: fast-
ing ,90 mg/dL, preprandial ,105 mg/dL,
1-h postprandial ,130–140 mg/dL, and
2-h postprandial ,120 mg/dL. If women
cannot achieve these targets without
significant hypoglycemia, the American
Diabetes Association (ADA) suggests
consideration of slightly higher targets:
fasting ,105 mg/dL, 1-h postprandial
,155 mg/dL, and 2-h postprandial
,130 mg/dL. Until harmonization of
these guidelines is achieved, the ADA
recommends setting targets based
on clinical experience, individualizing
care, as needed.
Diabetes Care Volume 38, Supplement 1, January 2015
Due to increases in red blood cell
turnover associated with pregnancy,
A1C levels fall during pregnancy. Addi-
tionally, as A1C represents an average, it
may not fully capture physiologically rel-
evant glycemic parameters in pregnancy.
A1C should be used as a secondary mea-
sure, next to self-monitoring of blood glu-
cose. The recommended A1C target in
pregnancy is ,6% if this can be achieved
without hypoglycemia. Given the alter-
ation in red blood cell kinetics during
pregnancy, A1C levels may need to be
monitored more frequently than usual
(e.g., monthly).
PREGNANCY AND
ANTIHYPERTENSIVE DRUGS
In a pregnancy complicated by diabetes
and chronic hypertension, target blood
pressure goals of systolic blood pres-
sure 110–129 mmHg and diastolic blood
pressure 65–79 mmHg are reasonable,
as they contribute to improved long-
term maternal health. Lower blood
pressure levels may be associated with
impaired fetal growth. During preg-
nancy, treatment with ACE inhibitors
and angiotensin receptor blockers is
contraindicated because they may
cause fetal damage. Antihypertensive
drugs known to be effective and safe in
pregnancy include methyldopa, labetalol,
diltiazem, clonidine, and prazosin.
Chronic diuretic use during pregnancy
has been associated with restricted ma-
ternal plasma volume, which may reduce
uteroplacental perfusion (8).
MANAGEMENT OF GESTATIONAL
DIABETES MELLITUS
As highlighted in Section 2. Classification
and Diagnosis of Diabetes, GDM is char-
acterized by increased risk of macrosomia
and birth complications, without a risk
threshold (9). Treatment starts with med-
ical nutrition therapy, exercise, and glu-
cose monitoring aiming for the targets
described previously. A total of 70 to
85% of women diagnosed with GDM un-
der older criteria can control GDM with
lifestyle modification alone; it is antici-
pated that this number will increase using
the lower International Association of the
Diabetes and Pregnancy Study Groups
(IADPSG) thresholds. Treatment has
been demonstrated to improve perinatal
outcomes in randomized studies and in a
U.S. Preventive Services Task Force re-
view (10). Historically, insulin has been
the recommended treatment for GDM
in the U.S. Randomized controlled trials
support the efficacy and short-term
safety of glyburide (11) (pregnancy cat-
egory B) and metformin (12,13) (preg-
nancy category B) for the treatment
of GDM. However, both agents cross
the placenta, and long-term safety
data are not available (14). Insulin also
may be used and should follow the
guidelines below.
MANAGEMENT OF
PREGESTATIONAL TYPE 1
DIABETES AND TYPE 2 DIABETES
IN PREGNANCY
Insulin Use in Pregnancy
Insulin is the preferred agent for man-
agement of diabetes in pregnancy be-
cause of the lack of long-term safety
data for noninsulin agents. The physiol-
ogy of pregnancy requires frequent ti-
tration of insulin to match changing
requirements. In the first trimester,
there is often a decrease in total daily
dose of insulin. In the second trimester,
rapidly increasing insulin resistance re-
quires weekly or biweekly increase in
insulin dose to achieve glycemic targets.
In general, a small proportion of the to-
tal daily dose should be given as basal
insulin and a greater proportion as pran-
dial insulin. Due to the complexity of
insulin management in pregnancy, re-
ferral to a specialized center is recom-
mended if this resource is available. All
insulins are pregnancy category B ex-
cept for glargine and glulisine, which
are labeled C.
Concerns Related to Type 1 Diabetes
in Pregnancy
Women with type 1 diabetes have an
increased risk of hypoglycemia in the
first trimester. Frequent hypoglycemia
can be associated with intrauterine
growth restriction. In addition, rapid im-
plementation of tight glycemic control
in the setting of retinopathy is associ-
ated with worsening of retinopathy
(15). Insulin resistance drops rapidly
with delivery of the placenta, and
women become very insulin sensitive,
requiring much less insulin than in the
prepartum period.
Concerns Related to Type 2 Diabetes
in Pregnancy
Pregestational type 2 diabetes is often
associated with obesity. Recommended
weight gain during pregnancy for
care.diabetesjournals.org
overweight women is 15–25 lb and for
obese women is 10–20 lb. Glycemic con-
trol is often easier to achieve in type 2
diabetes than in type 1 diabetes, but
hypertension and other comorbidities
often render pregestational type 2 dia-
betes as high or higher risk than preges-
tational type 1 diabetes (16,17).
POSTPARTUM CARE
Lactation
All women should be supported in at-
tempts to nurse their babies, given im-
mediate nutritional and immunological
benefits of breastfeeding for the baby;
there may also be a longer-term meta-
bolic benefit to both mother (18) and
offspring (19), though data are mixed.
Gestational Diabetes Mellitus
Because GDM may represent preexisting
undiagnosed type 2 diabetes, women
with GDM should be screened for persis-
tent diabetes or prediabetes at 6–12
weeks postpartum using nonpregnancy
criteria and every 1–3 years thereafter
depending on other risk factors. Women
with a history of GDM have a greatly in-
creased risk of conversion to type 2 dia-
betes over time and not solely within the
6–12 weeks’ postpartum time frame
(20). In the prospective Nurses’ Health
Study II (21), subsequent diabetes
risk after a history of GDM was signifi-
cantly lower in women who followed
healthy eating patterns. Adjusting for
BMI moderately, but not completely,
attenuated this association. Interpreg-
nancy or postpartum weight gain is as-
sociated with increased risk of adverse
pregnancy outcomes in subsequent
pregnancies (22) and earlier progression
to type 2 diabetes. Both metformin and
intensive lifestyle intervention prevent
or delay progression to diabetes in
women with a history of GDM. Of women
with a history of GDM and impaired glu-
cose tolerance, only 5–6 individuals need
to be treated with either intervention
to prevent one case of diabetes over
3 years (23).
Type 1 Diabetes
Insulin sensitivity increases in the imme-
diate postpartum period and then returns
to normal over the following 1–2 weeks,
and many women will require signifi-
cantly less insulin at this time than
during the prepartum period. Breast-
feeding may cause hypoglycemia, which
may be ameliorated by consuming a snack
(such as milk) prior to nursing. Diabetes
self-management often suffers in the
postpartum period.
Type 2 Diabetes
If the pregnancy has motivated the adop-
tion of a healthier diet, building on these
gains to support weight loss is recom-
mended in the postpartum period.
Contraception
All women of childbearing age, including
those who are postpartum, should have
contraception options reviewed at reg-
ular intervals.
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 S80 Diabetes Care Volume 38, Supplement 1, January 2015

American Diabetes Association

13. Diabetes Care in the Hospital,
Nursing Home, and Skilled Nursing
Facility
Diabetes Care 2015;38(Suppl. 1):S80–S85 | DOI: 10.2337/dc15-S016

Recommendations
POSITION STATEMENT

c Diabetes discharge planning should start at hospital admission, and clear

diabetes management instructions should be provided at discharge. E
c The sole use of sliding scale insulin (SSI) in the inpatient hospital setting is
strongly discouraged. A
c All patients with diabetes admitted to the hospital should have their diabetes
type clearly identified in the medical record. E
Critically Ill Patients
c Insulin therapy should be initiated for treatment of persistent hyperglycemia
starting at a threshold of no greater than 180 mg/dL (10 mmol/L). Once insulin
therapy is started, a glucose range of 140–180 mg/dL (7.8–10 mmol/L) is recom-
mended for the majority of critically ill patients. A
c More stringent goals, such as 110–140 mg/dL (6.1–7.8 mmol/L), may be
appropriate for selected patients, as long as this can be achieved without
significant hypoglycemia. C
c Critically ill patients require an intravenous insulin protocol that has demon-
strated efficacy and safety in achieving the desired glucose range without
increasing risk for severe hypoglycemia. E
Noncritically Ill Patients
c If treated with insulin, generally premeal blood glucose targets of ,140 mg/dL
(7.8 mmol/L) with random blood glucose ,180 mg/dL (10.0 mmol/L) are
reasonable, provided these targets can be safely achieved. More stringent
targets may be appropriate in stable patients with previous tight glycemic
control. Less stringent targets may be appropriate in those with severe co-
morbidities. C
c A basal plus correction insulin regimen is the preferred treatment for patients
with poor oral intake or who are taking nothing by mouth (NPO). An insulin
regimen with basal, nutritional, and correction components is the preferred
treatment for patients with good nutritional intake. A
c A hypoglycemia management protocol should be adopted and implemented by
each hospital or hospital system. A plan for preventing and treating hypoglycemia
should be established for each patient. Episodes of hypoglycemia in the hospital
should be documented in the medical record and tracked. E
c Consider obtaining an A1C in patients with diabetes admitted to the hospital if Suggested citation: American Diabetes Associa-
tion. Diabetes care in the hospital, nursing home,
the result of testing in the previous 3 months is not available. E
and skilled nursing facility. Sec. 13. In Standards
c Consider obtaining an A1C in patients with risk factors for undiagnosed of Medical Care in Diabetesd2015. Diabetes
diabetes who exhibit hyperglycemia in the hospital. E Care 2015;38(Suppl. 1):S80–S85
c Patients with hyperglycemia in the hospital who do not have a prior diagnosis © 2015 by the American Diabetes Association.
of diabetes should have appropriate follow-up testing and care documented at Readers may use this article as long as the work
discharge. E is properly cited, the use is educational and not
for profit, and the work is not altered.
care.diabetesjournals.org
HYPERGLYCEMIA IN THE HOSPITAL
Hyperglycemia in the hospital can re-
flect previously known or previously un-
diagnosed diabetes or may be hospital
related. The difficulty distinguishing be-
tween the second and third categories
during the hospitalization may be over-
come by measuring A1C, as long as con-
ditions interfering with A1C equilibrium
(such as hemolysis, blood transfusion,
blood loss, or erythropoietin therapy)
have not occurred. A1C values $6.5%
in undiagnosed patients suggest that
diabetes preceded hospitalization (1).
Hyperglycemia management in the hos-
pital has often been considered second-
ary in importance to the condition that
prompted admission. However, a body
of literature now supports targeted glu-
cose control in the hospital setting for
improved clinical outcomes (2). Hyper-
glycemia in the hospital may result
from stress or decompensation of
type 1, type 2, or other forms of diabe-
tes and/or may be iatrogenic due to with-
holding of antihyperglycemic medications
or administration of hyperglycemia-
provoking agents, such as glucocorticoids,
vasopressors, and enteral or parenteral
nutrition.
There is substantial observational
evidence linking hyperglycemia in hos-
pitalized patients (with or without dia-
betes) to poor outcomes. Cohort studies
as well as a few early randomized con-
trolled trials (RCTs) suggested that in-
tensive treatment of hyperglycemia
improved hospital outcomes (3,4). In
general, these studies were heteroge-
neous in terms of patient population,
blood glucose targets, insulin protocols,
provision of nutritional support, and the
proportion of patients receiving insulin,
which limits the ability to make mean-
ingful comparisons among them. Trials
in critically ill patients have failed to
show a significant improvement in mor-
tality with intensive glycemic control or
have even shown increased mortality
risk (5). Moreover, RCTs have high-
lighted the risk of severe hypoglycemia
resulting from such efforts (6–9).
The largest study to date, Normo-
glycemia in Intensive Care Evaluation-
Survival Using Glucose Algorithm
Regulation (NICE-SUGAR), a multicen-
ter, multinational RCT, compared the
effect of intensive glycemic control
(target 81–108 mg/dL [4.5–6.0 mmol/L];
mean blood glucose attained 115 mg/dL
[6.4 mmol/L]) to standard glycemic con-
trol (target 144–180 mg/dL [8.0–10.0
mmol/L]; mean blood glucose attained
144 mg/dL [8.0 mmol/L]) on outcomes
among 6,104 critically ill participants,
almost all of whom required mechanical
ventilation (6).
Ninety-day mortality was signifi-
cantly higher in the intensive versus
the conventional treatment group in
both surgical and medical patients, as
was mortality from cardiovascular
causes. Severe hypoglycemia was also
more common in the intensively treated
group (6.8% vs. 0.5%; P , 0.001).
The study results lie in stark contrast
to a 2001 single-center study that re-
ported a 42% relative reduction in inten-
sive care unit (ICU) mortality in critically ill
surgical patients treated to a target blood
glucose of 80–110 mg/dL (3). The NICE-
SUGAR findings do not disprove the no-
tion that glycemic control in the ICU is
important. However, they do strongly
suggest that it may not be necessary to
target blood glucose values ,140 mg/dL
(7.8 mmol/L) and that a highly stringent
target of ,110 mg/dL (6.1 mmol/L) may
actually be dangerous.
In a meta-analysis of 26 trials (n 5
13,567), which included the NICE-
SUGAR data, the pooled relative risk
[RR] of death with intensive insulin ther-
apy was 0.93 as compared with conven-
tional therapy (95% CI 0.83–1.04) (9).
Approximately half of these trials re-
ported hypoglycemia, with a pooled
RR of intensive therapy of 6.0 (95% CI
4.5–8.0). The specific ICU setting influ-
enced the findings, with patients in sur-
gical ICUs appearing to benefit from
intensive insulin therapy (RR 0.63 [95%
CI 0.44–0.91]), while those in other
medical and mixed critical care settings
did not. It was concluded that, overall,
intensive insulin therapy increased the
risk of hypoglycemia and provided no
overall benefit on mortality in the criti-
cally ill, although a possible mortality
benefit to patients admitted to the sur-
gical ICU was suggested.
GLYCEMIC TARGETS IN
HOSPITALIZED PATIENTS
Definition of Glucose Abnormalities in
the Hospital Setting
Hyperglycemia in the hospital has been de-
fined as any blood glucose .140 mg/dL
(7.8 mmol/L). Levels that are significantly
Position Statement S81
and persistently above this may re-
quire treatment in hospitalized pa-
tients. A1C values $6.5% suggest, in
undiagnosed patients, that diabetes
preceded hospitalization (1). Hypoglyce-
mia has been defined as any blood glu-
cose ,70 mg/dL (3.9 mmol/L). This is
the standard definition in outpatients
and correlates with the initial threshold
for the release of counterregulatory
hormones. Severe hypoglycemia in hos-
pitalized patients has been defined by
many as ,40 mg/dL (2.2 mmol/L),
although this is lower than the ;50
mg/dL (2.8 mmol/L) level at which cog-
nitive impairment begins in normal in-
dividuals (10). Both hyperglycemia and
hypoglycemia among inpatients are as-
sociated with adverse short- and long-
term outcomes. Early recognition and
treatment of mild to moderate hypogly-
cemia (40–69 mg/dL [2.2–3.8 mmol/L])
can prevent deterioration to a more
severe episode with potential adverse
sequelae (11).
Critically Ill Patients
Based on available evidence, for the ma-
jority of critically ill patients in the ICU
setting, intravenous insulin infusion
should be used to control hyperglyce-
mia, with a starting threshold of no
higher than 180 mg/dL (10.0 mmol/L).
Once intravenous insulin is started, the
glucose level should be maintained be-
tween 140–180 mg/dL (7.8–10.0 mmol/L).
Greater benefit may be realized at the
lower end of this range. Although strong
evidence is lacking, lower glucose targets
may be appropriate in select patients.
One small study suggested that ICU pa-
tients treated to targets of 120–140
mg/dL (6.7–7.8 mmol/L) had less nega-
tive nitrogen balance than those treated
to higher targets (12). However, targets
,110 mg/dL (6.1 mmol/L) are not rec-
ommended. Insulin infusion protocols
with demonstrated safety and efficacy,
resulting in low rates of hypoglycemia,
are highly recommended (11).
Noncritically Ill Patients
With no prospective RCT data to inform
specific glycemic targets in noncritically
ill patients, recommendations are
based on clinical experience and judg-
ment (13). For the majority of noncriti-
cally ill patients treated with insulin,
premeal glucose targets should gener-
ally be ,140 mg/dL (7.8 mmol/L) with
S82 Position Statement
random blood glucose ,180 mg/dL
(10.0 mmol/L), as long as these targets
can be safely achieved. To avoid hypo-
glycemia, consideration should be given
to reassessing the insulin regimen if
blood glucose levels fall below 100
mg/dL (5.6 mmol/L). Modifying the reg-
imen is required when blood glucose
values are ,70 mg/dL (3.9 mmol/L), un-
less the event is easily explained by
other factors (such as a missed meal).
There is some evidence that systematic
attention to hyperglycemia in the emer-
gency room leads to better glycemic
control in the hospital for those subse-
quently admitted (14).
Patients with a prior history of suc-
cessful tight glycemic control in the out-
patient setting who are clinically stable
may be maintained with a glucose range
below the aforementioned cut points.
Conversely, higher glucose ranges may
be acceptable in terminally ill patients or
in patients with severe comorbidities, as
well as in those in patient-care settings
where frequent glucose monitoring or
close nursing supervision is not feasible.
Clinical judgment combined with on-
going assessment of the patient’s clini-
cal status, including changes in the
trajectory of glucose measures, the se-
verity of illness, nutritional status, or
concomitant medications that might af-
fect glucose levels (e.g., glucocorticoids,
octreotide), must be incorporated into
the day-to-day decisions regarding insu-
lin dosing (11).
ANTIHYPERGLYCEMIC AGENTS IN
HOSPITALIZED PATIENTS
In most clinical situations in the hospital,
insulin therapy is the preferred method
of glycemic control (11). In the ICU, in-
travenous infusion is the preferred
route of insulin administration. When
the patient is transitioned off intrave-
nous insulin to subcutaneous therapy,
precautions should be taken to prevent
hyperglycemia (15,16). Outside of criti-
cal care units, scheduled subcutaneous
insulin that delivers basal, nutritional,
and correction components (basal–bolus
regimen) is recommended for patients
with good nutritional intake. A basal
plus correction insulin regimen is the
preferred treatment for patients with
poor oral intake or who are NPO. SSI
is strongly discouraged in hospitalized
patients as the sole method of insulin
treatment.
Diabetes Care Volume 38, Supplement 1, January 2015
For patients with type 1 diabetes,
dosing insulin solely based on premeal
glucose levels does not account for basal
insulin requirements or caloric intake,
increasing both hypoglycemia and hy-
perglycemia risks and potentially lead-
ing to diabetic ketoacidosis. It has
been shown in an RCT that basal–bolus
treatment improved glycemic control
and reduced hospital complications
compared with SSI in general surgery
patients with type 2 diabetes (17). Typ-
ical dosing schemes are based on body
weight, with some evidence that pa-
tients with renal insufficiency should
be treated with lower doses (18). The
reader is referred to publications and
reviews that describe available insulin
preparations and protocols and provide
guidance in the use of insulin therapy
in specific clinical settings, including
parenteral nutrition (19), enteral tube
feedings, and high-dose glucocorticoid
therapy (11).
Recent studies have investigated the
safety and efficacy of oral agents and in-
jectable noninsulin therapies, such as GLP-
1 analogs, in the hospital. A small study in
general medicine and surgical wards
showed that treatment with sitagliptin re-
sulted in similar glycemic control as a
basal–bolus regimen in patients with type
2 diabetes who had an A1C ,7.5% and, in
addition to a nutrition intervention, were
treated with oral agents or low doses of
insulin prior to hospitalization (20). Use of
intravenous exenatide infusion resulted in
improved glycemic control in patients ad-
mitted to a cardiac ICU (21). Further stud-
ies are needed to define the role of
incretin mimetics in the inpatient manage-
ment of hyperglycemia.
PREVENTING HYPOGLYCEMIA
Patients with or without diabetes may
experience hypoglycemia in the hospital
setting in association with altered nutri-
tional state, heart failure, renal or liver
disease, malignancy, infection, or sepsis.
Additional triggering events leading to
iatrogenic hypoglycemia include sudden
reduction of corticosteroid dose, altered
ability of the patient to report symp-
toms, reduced oral intake, emesis, new
NPO status, inappropriate timing of
short- or rapid-acting insulin in relation
to meals, reduced infusion rate of intra-
venous dextrose, and unexpected inter-
ruption of enteral feedings or parenteral
nutrition.
Despite the preventable nature of
many inpatient episodes of hypoglyce-
mia, institutions are more likely to have
nursing protocols for hypoglycemia treat-
ment than for its prevention. Tracking
such episodes and analyzing their causes
are important quality-improvement
activities (22).
DIABETES CARE PROVIDERS IN THE
HOSPITAL
Inpatient diabetes management may be
effectively championed and/or provided
by primary care physicians, endocrinol-
ogists, intensive care specialists, or hos-
pitalists. Involvement of appropriately
trained specialists or specialty teams
may reduce length of stay, improve gly-
cemic control, and improve outcomes
(11). Standardized orders for scheduled
and correction-dose insulin should be
implemented, while sole reliance on an
SSI regimen is strongly discouraged. As
hospitals move to comply with “mean-
ingful use” regulations for electronic
health records, as mandated by the
Health Information Technology for Eco-
nomic and Clinical Health Act, efforts
should be made to ensure that all com-
ponents of structured insulin order sets
are incorporated into electronic insulin
order sets (23,24).
To achieve glycemic targets associ-
ated with improved hospital outcomes,
hospitals will need a multidisciplinary
approach to develop insulin manage-
ment protocols that effectively and
safely enable achievement of glycemic
targets (25).
SELF-MANAGEMENT IN THE
HOSPITAL
Diabetes self-management in the hospi-
tal may be appropriate for competent
youth and adult patients who have a sta-
ble level of consciousness and reason-
ably stable daily insulin requirements,
successfully conduct self-management
of diabetes at home, have physical skills
needed to successfully self-administer
insulin and perform self-monitoring of
blood glucose, have adequate oral in-
take, are proficient in carbohydrate
counting, use multiple daily insulin in-
jections or insulin pump therapy, and
understand sick-day management. The
patient and physician, in consultation
with nursing staff, must agree that pa-
tient self-management is appropriate
while hospitalized.
care.diabetesjournals.org
Patients who use continuous subcuta-
neous insulin infusion (CSII) pump therapy
in the outpatient setting can be candi-
dates for diabetes self-management in
the hospital, provided that they have
the mental and physical capacity to do
so (11). Hospital policy and procedures
delineating inpatient guidelines for CSII
therapy are advisable, and availability of
hospital personnel with expertise in CSII
therapy is essential. It is important that
nursing personnel document basal rates
and bolus doses taken on a daily basis.
MEDICAL NUTRITION THERAPY IN
THE HOSPITAL
The goals of medical nutrition therapy
are to optimize glycemic control, pro-
vide adequate calories to meet meta-
bolic demands, and create a discharge
plan for follow-up care (2,26). The
American Diabetes Association (ADA)
does not endorse any single meal plan
or specified percentages of macronu-
trients, and the term “ADA diet” should
no longer be used. Current nutrition rec-
ommendations advise individualization
based on treatment goals, physiological
parameters, and medication use. Con-
sistent carbohydrate meal plans are
preferred by many hospitals as they fa-
cilitate matching the prandial insulin
dose to the amount of carbohydrate
consumed (27). Because of the complex-
ity of nutrition issues in the hospital, a
registered dietitian, knowledgeable and
skilled in medical nutrition therapy,
should serve as an inpatient team
member. The dietitian is responsible
for integrating information about the
patient’s clinical condition, meal plan-
ning, and lifestyle habits and for estab-
lishing treatment goals to determine a
realistic plan for nutrition therapy (28).
BEDSIDE BLOOD GLUCOSE
MONITORING
Bedside point-of-care (POC) blood glu-
cose monitoring is used to guide insulin
dosing. In the patient receiving nutri-
tion, the timing of glucose monitoring
should match carbohydrate exposure.
In the patient not receiving nutrition,
glucose monitoring is performed every
4–6 h (29,30). More frequent blood glu-
cose testing ranging from every 30 min
to every 2 h is required for patients on
intravenous insulin infusions.
Safety standards should be estab-
lished for blood glucose monitoring
that prohibit the sharing of finger-stick
lancing devices, lancets, needles, and me-
ters to reduce the risk of transmission of
blood-borne diseases. Shared lancing de-
vices carry essentially the same risk as
sharing syringes and needles (31).
Accuracy of blood glucose measure-
ments using POC meters has limitations
that must be considered. Although the
U.S. Food and Drug Administration cur-
rently allows a 620% error for blood
glucose meters, questions about the ap-
propriateness of these criteria have
been raised, especially for lower blood
glucose readings (32). Glucose mea-
sures differ significantly between plasma
and whole blood, terms that are often
used interchangeably and can lead to
misinterpretation. Most commercially
available capillary blood glucose meters
introduce a correction factor of ;1.12
to report a “plasma-adjusted” value (33).
Significant discrepancies between
capillary, venous, and arterial plasma
samples have been observed in patients
with low or high hemoglobin concentra-
tions, hypoperfusion, and interfering
substances such as maltose (contained
in immunoglobulins) (34). Analytical var-
iability has been described with several
meters (35). Increasingly, newer-generation
POC blood glucose meters correct for
variation in hematocrit and for interfer-
ing substances. Any glucose result that
does not correlate with the patient’s
status should be confirmed through
conventional laboratory sampling of
plasma glucose. The U.S. Food and Drug
Administration has become increasingly
concerned about POC blood glucose
meter use in the hospital and is presently
reviewing matters related to their use.
DISCHARGE PLANNING
Transition from the acute care setting
is a high-risk time for all patients, not
just those with diabetes or new hyper-
glycemia. Although there is extensive
literature concerning safe transition
within and from the hospital, little of it
is specific to diabetes (36). Diabetes dis-
charge planning is not a separate entity
but is an important part of an overall
discharge plan. As such, discharge plan-
ning begins at admission to the hospital
and is updated as projected patient
needs change.
Inpatients may be discharged to var-
ied settings, including home (with or
without visiting nurse services), assisted
Position Statement S83
living, rehabilitation, or skilled nursing
facilities. For the patient who is dis-
charged to assisted living or to home,
the optimal program will need to con-
sider the type and severity of diabetes,
the effects of the patient’s illness on
blood glucose levels, and the capacities
and desires of the patient. Smooth tran-
sition to outpatient care should be
ensured.
An outpatient follow-up visit with the
primary care provider, endocrinologist,
or diabetes educator within 1 month of
discharge is advised for all patients hav-
ing hyperglycemia in the hospital. Clear
communication with outpatient pro-
viders either directly or via hospital
discharge summaries facilitates safe
transitions to outpatient care. Providing
information regarding the cause of hy-
perglycemia (or the plan for determin-
ing the cause), related complications
and comorbidities, and recommended
treatments can assist outpatient pro-
viders as they assume ongoing care.
The Agency for Healthcare Research
and Quality recommends that, at a
minimum, discharge plans include the
following:
Medication Reconciliation
○ The patient’s medications must be
cross-checked to ensure that no
chronic medications were stopped
and to ensure the safety of new
prescriptions.
○ Prescriptions for new or changed
medication should be filled and re-
viewed with the patient and family
at or before discharge.
Structured Discharge Communication
○ Information on medication changes,
pending tests and studies, and follow-
up needs must be accurately and
promptly communicated to outpatient
physicians.
○ Discharge summaries should be trans-
mitted to the primary physician as soon
as possible after discharge.
○ Appointment-keeping behavior is
enhanced when the inpatient team
schedules outpatient medical follow-
up prior to discharge. Ideally, the inpa-
tient care providers or case managers/
discharge planners will schedule
follow-up visit(s) with the appropriate
professionals, including primary care
provider, endocrinologist, and diabetes
educator (37).
S84 Position Statement
DIABETES SELF-MANAGEMENT
EDUCATION
Teaching diabetes self-management to
patients in hospitals is a challenging
task. Patients are ill, under increased
stress related to their hospitalization
and diagnosis, and in an environment
not conducive to learning. Ideally, people
with diabetes should be taught at a time
and place conducive to learning: as an
outpatient in a recognized program of di-
abetes education. For the hospitalized pa-
tient, diabetes “survival skills” education
is generally a feasible approach to provide
sufficient information and training to en-
able safe care at home. Patients hospital-
ized because of a crisis related to diabetes
management or poor care at home re-
quire education to prevent subsequent
episodes of hospitalization. Assessing
the need for a home health referral
or referral to an outpatient diabetes ed-
ucation program should be part of
discharge planning for all patients. Ex-
panded diabetes education can be ar-
ranged in the community.
Diabetes self-management education
should start upon admission or as soon
as feasible, especially in those new to
insulin therapy or in whom the diabetes
regimen has been substantially altered
during the hospitalization.
It is recommended that the following
areas of knowledge be reviewed and ad-
dressed prior to hospital discharge:
○ Identification of the health care pro-
vider who will provide diabetes care
after discharge
○ Level of understanding related to the
diagnosis of diabetes, self-monitoring
of blood glucose, and explanation of
home blood glucose goals
○ Definition, recognition, treatment,
and prevention of hyperglycemia
and hypoglycemia
○ Information on consistent eating pat-
terns
○ When and how to take blood
glucose–lowering medications, in-
cluding insulin administration (if go-
ing home on insulin)
○ Sick-day management
○ Proper use and disposal of needles
and syringes
It is important that patients be pro-
vided with appropriate durable medi-
cal equipment, medication, supplies,
and prescriptions at the time of
Diabetes Care Volume 38, Supplement 1, January 2015
discharge in order to avoid a poten-
tially dangerous hiatus in care. These
supplies/prescriptions should include
the following:
○ Insulin (vials or pens), if needed
○ Syringes or pen needles, if needed
○ Oral medications, if needed
○ Blood glucose meter and strips
○ Lancets and lancing devices
○ Urine ketone strips (type 1 diabetes)
○ Glucagon emergency kit (insulin-
treated patients)
○ Medical alert application/charms
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and the Endocrine Society. Diabetes Care
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23. Schnipper JL, Liang CL, Ndumele CD,
Pendergrass ML. Effects of a computerized or-
der set on the inpatient management of hyper-
glycemia: a cluster-randomized controlled trial.
Endocr Pract 2010;16:209–218
24. Wexler DJ, Shrader P, Burns SM, Cagliero E.
Effectiveness of a computerized insulin order
template in general medical inpatients with
type 2 diabetes: a cluster randomized trial. Di-
abetes Care 2010;33:2181–2183
25. Furnary AP, Braithwaite SS. Effects of out-
come on in-hospital transition from intravenous
insulin infusion to subcutaneous therapy. Am J
Cardiol 2006;98:557–564
care.diabetesjournals.org
26. Schafer RG, Bohannon B, Franz MJ, et al.;
American Diabetes Association. Diabetes
nutrition recommendations for health care in-
stitutions. Diabetes Care 2004;27(Suppl. 1):
S55–S57
27. Curll M, Dinardo M, Noschese M,
Korytkowski MT. Menu selection, glycaemic
control and satisfaction with standard and
patient-controlled consistent carbohydrate
meal plans in hospitalised patients with diabe-
tes. Qual Saf Health Care 2010;19:355–359
28. Evert AB, Boucher JL, Cypress M, et al. Nu-
trition therapy recommendations for the man-
agement of adults with diabetes. Diabetes Care
2014;37(Suppl. 1):S120–S143
29. Korytkowski MT, Salata RJ, Koerbel GL,
et al. Insulin therapy and glycemic control
in hospitalized patients with diabetes during
enteral nutrition therapy: a randomized controlled
clinical trial. Diabetes Care 2009;32:594–596
30. Umpierrez GE. Basal versus sliding-scale
regular insulin in hospitalized patients with hy-
perglycemia during enteral nutrition therapy.
Diabetes Care 2009;32:751–753
31. Klonoff DC, Perz JF. Assisted monitoring of
blood glucose: special safety needs for a new
paradigm in testing glucose. J Diabetes Sci
Tech 2010;4:1027–1031
32. Vandvik PO, Lincoff AM, Gore JM, et al.;
American College of Chest Physicians. Primary
and secondary prevention of cardiovascular dis-
ease: Antithrombotic Therapy and Prevention of
Thrombosis, 9th ed: American College of Chest
Physicians Evidence-Based Clinical Practice Guide-
lines. Chest 2012;141(Suppl.):e637S–e668S
33. D’Orazio P, Burnett RW, Fogh-Andersen N,
et al.; International Federation of Clinical Chem-
istry Scientific Division Working Group on Selec-
tive Electrodes and Point of Care Testing.
Approved IFCC recommendation on reporting
Position Statement S85
results for blood glucose (abbreviated). Clin
Chem 2005;51:1573–1576
34. Dungan K, Chapman J, Braithwaite SS, Buse
J. Glucose measurement: confounding issues in
setting targets for inpatient management. Dia-
betes Care 2007;30:403–409
35. Boyd JC, Bruns DE. Quality specifications for
glucose meters: assessment by simulation mod-
eling of errors in insulin dose. Clin Chem 2001;
47:209–214
36. Shepperd S, Lannin NA, Clemson LM,
McCluskey A, Cameron ID, Barras SL. Discharge
planning from hospital to home. Cochrane Da-
tabase Syst Rev 2013;1:CD000313
37. Agency for Healthcare Research and Qual-
ity. AHRQ Patient Safety Networkdadverse
events after hospital discharge [Internet],
2014. Available from http://psnet.ahrq.gov/
primer.aspx?primerID511. Accessed 1 October
2014
 S86 Diabetes Care Volume 38, Supplement 1, January 2015

American Diabetes Association

14. Diabetes Advocacy
Diabetes Care 2015;38(Suppl. 1):S86–S87 | DOI: 10.2337/dc15-S017

Managing the daily health demands of diabetes can be challenging. People living
with diabetes should not have to face additional discrimination due to diabetes. By
advocating for the rights of those with diabetes at all levels, the American Diabetes
Association (ADA) can help ensure that they live a healthy and productive life. A
strategic goal of the ADA is that by the end of 2015, more children and adults with
diabetes will be living free from the burden of discrimination.
One tactic for achieving this goal is to implement the ADA’s Standards of Medical
Care through advocacy-oriented position statements. The ADA publishes evidence-
based, peer-reviewed statements on topics such as diabetes and employment, di-
abetes and driving, and diabetes management in certain settings such as schools,
child care programs, and correctional institutions. In addition to ADA’s clinical
position statements, these advocacy position statements are important tools in
POSITION STATEMENT

educating schools, employers, licensing agencies, policy makers, and others about
the intersection of diabetes medicine and the law.
ADVOCACY POSITION STATEMENTS
Partial list, with most recent publications appearing first
Care of Young Children With Diabetes in the Child Care Setting (1)
First publication: 2014
Very young children (aged ,6 years) with diabetes have legal protections and can
be safely cared for by child care providers with appropriate training, access to resources,
and a system of communication with parents and the child’s diabetes provider. See
the ADA position statement “Care of Young Children With Diabetes in the Child Care Set-
ting” for further discussion: http://care.diabetesjournals.org/content/37/10/2834.
Diabetes and Driving (2)
First publication: 2012
People with diabetes who wish to operate motor vehicles are subject to a great variety of
licensing requirements applied by both state and federal jurisdictions, which may lead to
loss of employment or significant restrictions on a person’s license. Presence of a medical
condition that can lead to significantly impaired consciousness or cognition may lead to
drivers being evaluated for fitness to drive. People with diabetes should be individually
assessed by a health care professional knowledgeable in diabetes if license restrictions
are being considered, and patients should be counseled about detecting and avoiding
hypoglycemia while driving. See the ADA position statement “Diabetes and Driving” for
further discussion: http://care.diabetesjournals.org/content/37/Supplement_1/S97.
Diabetes and Employment (3)
First publication: 1984 (revised 2009)
Any person with diabetes, whether insulin-treated or noninsulin-treated, should be
eligible for any employment for which he or she is otherwise qualified. Employment
decisions should never be based on generalizations or stereotypes regarding the
effects of diabetes. When questions arise about the medical fitness of a person with
diabetes for a particular job, a health care professional with expertise in treating
diabetes should perform an individualized assessment. See the ADA position statement
“Diabetes and Employment” for further discussion: http://care.diabetesjournals.org/
Suggested citation: American Diabetes Associa-
content/37/Supplement_1/S112. tion. Diabetes advocacy. Sec. 14. In Standards of
Diabetes Care in the School and Day Care Setting (4)* Medical Care in Diabetesd2015. Diabetes Care
2015;38(Suppl. 1):S86–S87
First publication: 1998 (revised 2008)
© 2015 by the American Diabetes Association.
As a sizeable portion of a child’s day is spent in school, close communication with and Readers may use this article as long as the work
cooperation of school personnel are essential for optimal diabetes management, is properly cited, the use is educational and not
safety, and maximal academic opportunities. See the ADA position statement “Diabetes for profit, and the work is not altered.
care.diabetesjournals.org
Care in the School and Day Care Setting”
for further discussion: http://care
.diabetesjournals.org/content/37/
Supplement_1/S91.
*In October 2014, a separate statement
on the care of young children with diabetes
in the child care setting was published.
Diabetes Management in Correctional
Institutions (5)
First publication: 1989 (revised 2008)
People with diabetes in correctional facili-
ties should receive care that meets na-
tional standards. Because it is estimated
that nearly 80,000 inmates have diabetes,
correctional institutions should have writ-
ten policies and procedures for the man-
agement of diabetes and for training of
medical and correctional staff in diabetes
care practices. See the ADA position
statement “Diabetes Management in
Correctional Institutions” for further dis-
cussion: http://care.diabetesjournals
.org/content/37/Supplement_1/S104.
References
1. Siminerio LM, Albanese-O’Neill A, Chiang JL,
et al. Care of young children with diabetes in the
Position Statement S87
child care setting: a position statement of the
American Diabetes Association. Diabetes Care
2014;37:2834–2842
2. American Diabetes Association. Diabetes
and driving. Diabetes Care 2014;37(Suppl. 1):
S972S103
3. American Diabetes Association. Diabetes
and employment. Diabetes Care 2014;37(Suppl.
1):S112–S117
4. American Diabetes Association. Diabetes
care in the school and day care setting. Diabetes
Care 2014;37(Suppl. 1):S91–S96
5. American Diabetes Association. Diabetes
management in correctional institutions.
Diabetes Care 2014;37(Suppl. 1):S104–
S111
PROFESSIONAL PRACTICE COMMITTEE

S88 Diabetes Care Volume 38, Supplement 1, January 2015

Professional Practice Committee

for the Standards of Medical Care
in Diabetesd2015
Diabetes Care 2015;38(Suppl. 1):S88–S89 | DOI: 10.2337/dc15-S018

Committee members disclosed the following financial or other conflicts of interest covering the period 12 months before
7 September 2014
Member Employment Research grant Other research support
Richard W. Grant, MD, MPH (Chair) Division of Research, Kaiser NIDDK, NHLBI None
Permanente, Oakland, CA
Thomas W. Donner, MD Johns Hopkins University School of Novo Nordisk*# None
Medicine, Baltimore, MD
Judith E. Fradkin, MD National Institutes of Health, None None
Bethesda, MD
Charlotte Hayes, MMSc, MS, RD, Private practice: (NF)2 Nutrition and None None
CDE, ACSM CES Fitness Consulting, Atlanta, GA
William H. Herman, MD, MPH University of Michigan, Ann Arbor, MI None None
William C. Hsu, MD Joslin Diabetes Center, Boston, MA None None
Eileen Kim, MD Kaiser Permanente Northern None None
California Region, Oakland, CA
Lori Laffel, MD, MPH Joslin Diabetes Center and Harvard Dexcom, Boehringer None
Medical School, Boston, MA Ingelheim
Rodica Pop-Busui, MD, PhD University of Michigan, Ann Arbor, MI NHLBI, NIDDK, ADA, None
Bristol-Myers Squibb
Neda Rasouli, MD University of Colorado, Denver, CO Novo Nordisk,# Bristol- None
Myers Squibb,# Merck
Sharp & Dohme,# NIDDK,#
Pfizer#
Desmond Schatz, MD University of Florida, Gainesville, FL None NIDDK, NIAID, Jaeb
Center for Health
Research, JDRF, Helmsley
Charitable Trust
Joseph A. Stankaitis, MD, MPH Monroe Plan for Medical Care, Milbank Memorial Fund None
Rochester, NY
Tracey H. Taveira, PharmD, University of Rhode Island College of AHA None
CDOE, CVDOE Pharmacy, Kingston, RI; Providence VA
Medical Center, Warren Alpert
Medical School of Brown University,
Providence, RI
Deborah J. Wexler, MD Massachusetts General Hospital, NIDDK None
Boston, MA
Jane L. Chiang, MD (Staff) ADA, Alexandria, VA None None
Erika Gebel Berg, PhD (Staff) ADA, Alexandria, VA None None
ADA, American Diabetes Association; AHA, American Heart Association; MEDCAC, Medicare Evidence Development & Coverage Advisory
Committee; NHLBI, National Heart, Lung, and Blood Institute; NIAID, National Institute of Allergy and Infectious Diseases; NIDDK, National Institute
of Diabetes and Digestive and Kidney Diseases.
*$$10,000 per year from company to individual.
#Grant or contract is to university or other employer.
care.diabetesjournals.org Professional Practice Committee S89

Speakers’ bureau/ Ownership

Member honoraria interest Consultant/advisory board Other
R.W.G. None None None None
T.W.D. None None None None
J.E.F. None None None None
C.H. Scherer Clinical None Emory University, Emory Diabetes Receives royalties from the ADA,
Communications Course at Grady, Team Novo Nordisk Academy of Nutrition and Dietetics
(Chair, Legislative and Public Policy
Committee)
W.H.H. None None AstraZeneca, Novo Nordisk (self and National Committee for Quality
spouse), Merck Sharp & Dohme,* GI Assurance (Chair, Diabetes Panel),
Dynamics, Boehringer Ingelheim Centers for Medicare & Medicaid
Services (member, MEDCAC),
Diabetic Medicine (Editor for the
Americas)
W.C.H. None None Novo Nordisk None
E.K. None None None None
L.L. None None Johnson & Johnson, Eli Lilly, Sanofi, None
Bristol-Myers Squibb, Menarini,
Novo Nordisk, AstraZeneca, LifeScan/
Animas, Boehringer Ingelheim,
Dexcom
R.P.-B. None None Acorda Therapeutics, AstraZeneca, None
T1D Exchange
N.R. None None None None
D.S. None None Daiichi Sankyo, Andromeda Biotech ADA Board of Directors, ADA officer
J.A.S. None None TPG National Payor Roundtable, National Committee for Quality
Amgen, Celgene, Gilead, Salix Assurance (physician surveyor and
Pharmaceuticals, Janssen member of Reconsideration
Pharmaceuticals, Bayer, Medtronic Committee), New York State
Department of Health Medicaid
Redesign Team’s Evidence-Based
Benefit Review Workgroup, Board
member (Chair-Elect) for St. Ann’s
Community, Rochester, NY, a non-
profit senior living/long-term care
organization
T.H.T. None None None None
D.J.W. None None None Diabetes Care (Editorial Board)
J.L.C. None None None None
E.G.B. None None None None
 S90 Diabetes Care Volume 38, Supplement 1, January 2015

Index

A1C. see also glycemic targets cardiovascular disease changes, initiatives, S6

CGM, S34 A1C relationship to, S36 demographic changes, S5
children and adolescents, S35, S71 autonomic neuropathy, S25, S62–S63 improvement strategies, S5
glycemic target determination, S37 children and adolescents, S72 patient-centeredness, S5
goals, S35 dietary fat management, S23–S24 regime reevaluation, S6–S7
limitations, S34–S35 patient-centeredness, S5 resources, S6
macrovascular complications, S36 pharmacological therapy, S51–S55, S59 clonidine, S78
mean glucose levels, S35 postprandial plasma glucose testing, S37 clopidogrel, S54, S55
microvascular complications, S35–S36 revisions summary, S4 cognitive impairment, S19, S38, S70
race/ethnicity differences, S9, S35 risk calculator, S52 colesevelam, S42, S44
recommendations, S34, S35, S37 risk factors, S10, S12, S25, S32 comorbidities, S17–S19, S26
SMBG, S33–S34 risk management, S49–S55 congestive heart failure, S51, S55
testing, S8–S10, S12, S34–S35 screening, S31, S55 consensus reports, S1
acarbose, S44 testing frequency, S9 continuous glucose monitoring (CGM), S4,
ACCORD trial, S19, S36, S38, S50, S53 Care of Young Children With Diabetes in the S33, S34
A1C Derived Average Glucose (ADAG) trial, Child Care Setting, S86 continuous subcutaneous insulin infusion
S35, S37 celiac disease, S71 (CSII), S83
ACE inhibitors, S49–S51, S55, S58–S60, Charcot foot, S64 contraception, S79
S72, S78 children and adolescents coronary heart disease, S55
acute coronary syndrome, S54, S55 A1C goals, S35, S71 cystic fibrosis–related diabetes, S15
adolescents. see children and autoimmune conditions, S71
adolescents cardiovascular disease, S72 dapagliflozin, S45
ADVANCE-BP trial, S50, S51 celiac disease, S71 Da Qing study, S31
ADVANCE trial, S36, S38 cognitive impairment, S70 DAWN2 study, S26
advocacy, S5, S86–S87 DSME/DSMS, S73 day care, S73, S86–S87
African Americans, S9, S11, S12, S24, S35 dyslipidemia, S72 degludec, S45
age. see older adults family stresses, S74 depression, S18, S26, S67, S74
AIM-HIGH trial, S53 glycemic control, S70–S71 detemir, S45
albiglutide, S45 hypertension, S71–S72 Diabetes and Driving, S86
albuminuria, S25, S58–S60, S73 hypoglycemia, S70 Diabetes and Employment, S86
alcohol, S23, S51 nephropathy, S72–S73 Diabetes Care in the School and Day Care
alogliptin, S44 neuropathy, S73 Setting, S86–S87
amlodipine, S51 pediatric to adult care transition, Diabetes Control and Complications Trial
amputations, S63–S64 S73–S74 (DCCT), S35, S36, S38, S41, S70
amylin mimetics, S45 plasma blood glucose goals, S71 Diabetes Management in Correctional
anemia, S9 psychosocial issues, S74 Institutions, S87
angiotensin receptor blockers (ARBs), resources, S86 Diabetes Prevention Program (DPP),
S49–S51, S55, S58–S60, S72, S78 retinopathy, S73 S31, S32
ankle-brachial index (ABI), S63, S64 revisions summary, S4 Diabetes Prevention Program Outcomes
antihypertensive medications, S51, school, child care, S73 Study (DPPOS), S31, S32
S59, S78 smoking, S72 diabetes-related distress, S26
antiplatelet agents, S54–S55, S61 statins, S72 diabetes self-management education
Antithrombotic Trialists’ (ATT) Collaboration, S54 thyroid disease, S71 (DSME)
Asian Americans, S9–S12 type 1 diabetes, S10–S11, S70–S74 benefits, S6, S20–S21
aspart, S43, S45 type 2 diabetes, S12–S13, S74 carbohydrate management, S21–S23
aspirin resistance, S55 chlorthalidone, S51 children and adolescents, S73
aspirin therapy, S54–S55, S61 cholesterol. see also dyslipidemia dietary fat management, S23–S24
assisted living. see hospital care children and adolescents, S72 eating patterns, S21–S23
autoimmune disease, S10–S11 control, S51 herbal supplements, S23
Automation to Simulate Pancreatic Insulin monitoring, S53 hospital care, S84
Response (ASPIRE) trial, S34 screening, S10, S52 medical nutrition therapy, S21–S23, S52,
autonomic neuropathy, S25, S62–S63 treatment, S52, S55 S72, S83
Chronic Care Model (CCM), S5, S6 micronutrients, S23
bariatric surgery, S46–S47 chronic kidney disease, S23, S25, S58–S60 national standards, S21
benazepril, S51 classification, diagnosis overview, S17, S20–S21
biguanides, S31, S32, S42–S44 overview, S8 prediabetes, S32
bile acid sequestrants, S42, S44, S53 prediabetes, S9–S10, S12–S13 protein management, S22, S23, S59
b-blockers, S51, S55 revisions summary, S4 recommendations, S20, S31
blood pressure control. see hypertension testing, S8–S10 reimbursement, S21
body mass index (BMI), S12 testing frequency, S9 sodium, S23, S24, S51
INDEX

bromocriptine, S42, S45 claudication, S63 weight loss, S21, S55

clinical management diabetes self-management support (DSMS).
calcium channel blockers, S51, S59 advocacy, S5, S86–S87 see diabetes self-management education
canagliflozin, S45 behavior change support, S6 (DSME)
cancer, S18 behavior optimization, S6 Diabetic Retinopathy Study (DRS), S61
carbohydrates, S21–S23 care delivery systems, S6 diastolic blood pressure goals, S4
care.diabetesjournals.org Index S91

diet, nutrition, S21–S23 postpartum care, S79 diastolic blood pressure, S50–S51
diltiazem, S78 recommendations, S13 goals, S49, S50
dipeptidyl peptidase 4 (DPP-4) inhibitors, screening, S10 lifestyle modification, S49, S51
S42–S44, S46, S68 two-step strategy, S13–S14 older adults, S67
disordered eating, S74 glargine, S45 overview, S49–S50
diuretics, S49–S51, S58, S59, S78 gliclazide, S44 pharmacological therapy, S49–S51
dopamine-2 agonists, S45 glimepiride, S44 recommendations, S49
driving, S86 glipizide, S44 screening, S10, S49, S50
dulaglutide, S45 glucagon, S38 sodium guidelines, S24, S51
dyslipidemia. see also cholesterol; glucagon-like peptide 1 (GLP-1) agonists, S42, systolic blood pressure, S50, S59
triglycerides S43, S45, S46, S68, S82 treatment, S49, S50
children and adolescents, S72 a-glucosidase inhibitors, S42, S44 Hypertension Optimal Treatment (HOT) trial, S50
control, S51 glulisine, S43, S45 hypertriglyceridemia, S53
lifestyle modification, S52, S55 glyburide/glibenclamide, S44 hypoglycemia
monitoring recommendations, S4, S53 glycemic targets. see also A1C A1C goals, S35, S37
recommendations, S51–S52 A1C/microvascular complications CGM, S34
screening, S51 relationships, S35–S36 children and adolescents, S70
treatment, S52–S55 determination, S37 exercise, S25
glycemic control assessment, S33–S35 hospital care, S80–S82
Early Treatment Diabetic Retinopathy Study hospital care, S80–S82 nocturnal, S34
(ETDRS), S61 intercurrent illness, S39 older adults, S68
eating abnormalities, S74 mean glucose levels, S35 overview, S38
eating patterns, S21–S23 mortality findings, S36 pregnancy, S78
e-cigarettes, S4, S25 older adults, S68 prevention, S38, S82
empagliflozin, S45 pregnancy, S77, S78 recommendations, S38
employment, S86 recommendations, S33, S36–S37 treatment, S38
end-stage renal disease (ESRD), S59 revisions summary, S4 hypoglycemia unawareness
Epidemiology of Diabetes Interventions and glycemic treatment approaches CGM, S33, S34
Complications (EDIC) study, S35–S36, S38 bariatric surgery, S46–S47 children and adolescents, S70
erectile dysfunction, S63 pharmacological therapy, S41–S46 effects, characterization, S38
exenatide/exenatide ER, S45, S82 revisions summary, S4 recommendations, S38
exercise gram-positive cocci, S64
albuminuria, S25 immune-mediated diabetes, S10–S11
autonomic neuropathy, S25, S62–S63 hearing impairment, S19 immunization recommendations, S4,
benefits, S24 hemoglobinopathies, S9 S26–S27
children, S24 hepatitis B vaccination, S26 impaired fasting glucose (IFG), S10, S31
frequency, type, S24 herbal supplements, S23 impaired glucose tolerance (IGT), S10, S31
glycemic control, S24 hospital care incretin-based therapies, S42
hyperglycemia, S25 bedside blood glucose monitoring, S83 indapamide, S50, S51
hypoglycemia, S25 critically ill patients, S80, S81 infections, S64
kidney disease, S23, S25, S58–S60, discharge planning, S80, S83 influenza vaccine, S26–S27
S72–S73 DSME, S84 insulin
peripheral neuropathy, S25, S62–S63 glucose abnormalities definitions, S81 basal–bolus, S43, S45, S46, S70,
prediabetes, S24 glycemic targets, S80–S82 S71, S82
pre-exercise evaluation, S24–S25 hyperglycemia, S80–S81 combination therapy, S42
recommendations, S24 hypoglycemia, S80–S82 glycemic targets, S38
retinopathy, S25, S60–S62, S73 insulin therapy, S80–S82 hospital care, S80–S82
ezetimibe, S53 management team, S82 hypoglycemia treatment, S38
medical nutrition therapy, S83 intensive insulin regimens, S34
fasting plasma glucose testing, S9 medication reconciliation, S83 MDI, S41
fatty liver disease, S18 non critically ill patients, S80–S82 older adults, S68
fenofibrate, S53 recommendations, S80 pregnancy, S78
fibrates, S53 self-management, S82–S83 recommendations, S33
Finnish Diabetes Prevention Study (DPS), S31 sliding scale insulin (SSI), S80, S82 sliding scale insulin (SSI), S80, S82
foot care, S4, S63–S64 structured discharge communication, S83 type 1 diabetes, S41
foot infections, S64 type 1 diabetes, S82 type 2 diabetes, S42–S46
foundations of care revisions summary, S4 hydrochlorothiazide, S51 insulin dependent diabetes, S10–S11
fractures, S18–S19 hyperglycemia insulin pump therapy, S33, S41, S43, S83
FRAX score, S18 cognitive impairment, S19 insulin resistance, S10, S78
fundus photographs, S61 exercise, S25 insulin secretagogues, S38, S68
glycemic target determination, S37 International Association of the Diabetes
gastrointestinal neuropathies, S62 hospital care, S80–S81 and Pregnancy Study Groups
gastroparesis, S63 older adults, S67, S68 (IADPSG), S13
genitourinary tract disturbances, S62–S63 plasma glucose testing, S9
gestational diabetes mellitus (GDM). see also postprandial, S37 jail, S87
pregnancy risk factors, S11 juvenile-onset diabetes, S10–S11
classification, S8 Hyperglycemia and Adverse Pregnancy
diagnosis, S13–S14 Outcome (HAPO) study, S13 kidney disease, S23, S25, S58–S60, S72–S73
glycemic targets, S77, S78 hyperglycemic crisis, S9 Kumamoto Study, S36
management, S78 hypertension
one-step strategy, S13, S14 children and adolescents, S71–S72 labetalol, S78
overview, S13, S77 diagnosis, S49, S50 lactation, S79
S92 Index Diabetes Care Volume 38, Supplement 1, January 2015

laser photocoagulation therapy, S61–S62 hypoglycemia, S68 repaglinide, S44

lifestyle modifications pharmacological therapy, S68–S69 retinal photography, S61
dyslipidemia, S52, S55 recommendations, S67 retinopathy, S25, S60–S62, S73
hypertension, S49, S51 sodium guidelines, S24 revisions summary, S4
type 2 diabetes, S31, S42 statin therapy, S52, S53 Reye syndrome, S54
linagliptin, S44 treatment goals, S67–S68 risk management, S4, S6, S9, S11
liraglutide, S45 type 2 diabetes screening, S12 rosiglitazone, S44
lispro, S43, S45 orthostatic hypotension, S63
lixisenatide, S45 overweight, obesity, S9, S10, S21, S55, SAVOR-TIMI 53 trial, S68–S69
Look AHEAD trial, S18, S55 S78–S79 saxagliptin, S44, S68–S69
loss of protective sensation (LOPS), school, S73, S86–S87
S63, S64 Patient-Centered Medical Home, S6 scientific evidence grading,
perindopril, S50, S51 S1–S2
macrovascular complications, S35, S36, S51 periodontal disease, S19 scientific statements, S1
macular edema, S61 peripheral arterial disease, S63, S64 self-monitoring of blood glucose
management planning, S17–S19, S26 peripheral neuropathy, S25, S62–S63 (SMBG)
maturity-onset diabetes of the young pharmacological therapy basal insulin/oral agents, S34
(MODY), S14 cardiovascular disease, S51–S55, S59 intensive insulin regimens, S34
medical evaluation, S17, S18, S24–S25 hypertension, S49–S51 optimization, S33–S34
medical nutrition therapy, S21–S23, S52, S72, microvascular complications, S51 overview, S33
S83 older adults, S68–S69 recommendations, S33
Medicare/Medicaid, S21 prediabetes, S32 sickle cell trait, S9
medications, S12. see also pharmacological type 2 diabetes, S31–S32, S42–S46 sitagliptin, S44, S82
therapy; specific medications, conditions pioglitazone, S44, S46 skilled nursing facilities. see hospital care
meglitinides, S42, S44 pneumococcal polysaccharide vaccine 23 sliding scale insulin (SSI), S80, S82
mental health specialist referrals, S26 (PPSV23), S26, S27 smoking, S4, S25, S63, S72
metformin, S31, S32, S42–S44, S55, S59, polycystic ovary syndrome, S10 sodium, S23, S24, S51
S68 position statements, S1 sodium–glucose cotransporter 2 (SGLT2)
methyldopa, S78 pramlintide, S41–S42, S45 inhibitors, S42, S43, S45, S46
microvascular complications prasugrel, S55 Standards of Care recommendations, S1
A1C goals, S35 prazosin, S78 Staphylococci, S64
A1C relationship to, S35–S36 prediabetes statins, S4, S52–S55, S72
erectile dysfunction, S63 classification, diagnosis, S9–S10, stroke, S36, S54, S59
gastroparesis, S63 S12–S13 sulfonylureas
glycemic control, S63 DSME/DSMS, S32 A1C/CVD relationships, S36
kidney disease, S23, S25, S58–S60, exercise, S24 combination therapy, S42, S43
S72–S73 pharmacological therapy, S32 older adults, S68
neuropathy, S25, S62–S63, S73 pre-exercise medical evaluation, S24–S25 type 2 diabetes, S43, S44, S46
orthostatic hypotension, S63 pregnancy
patient education, S64 A1C testing, S9, S78 testosterone levels, S19
pharmacological therapy, S51 antihypertensive medications, S51, thiazolidinediones, S43, S44, S46
retinopathy, S25, S60–S62, S73 S78 thyroid disease, S71
revisions summary, S4 contraception, S79 ticagrelor, S55
risk factors, S11 GDM (see gestational diabetes mellitus triglycerides, S10, S52, S53. see also
miglitol, S44 [GDM]) dyslipidemia
monogenic diabetes syndromes, S14–S15 glycemic targets, S77, S78 2-hour plasma glucose testing, S9
myocardial infarction (MI), S36, S50, S54, S55, hypertension, S50 type 1 diabetes
S59 hypoglycemia, S78 A1C/mean glucose relationship,
insulin, S78 S35
nateglinide, S44 insulin resistance, S78 autoimmune conditions, S71
National Diabetes Education Program (NDEP), lactation, S79 carbohydrate management, S21
S6, S74 medications contraindicated, S77, S78 CGM, S33, S34
National Diabetes Prevention Program, S31 metabolic physiology, S78 children and adolescents, S10–S11,
National Institutes of Health (NIH), overweight, obesity, S78–S79 S70–S74
S13–S14 postpartum care, S79 classification, S8
neonatal diabetes, S14 preconception counseling, S77 diagnosis, S10–S11
nephropathy, S23, S25, S58–S60, S72–S73 recommendations, S77 glycemic control,
neuropathy, S25, S62–S63, S73 retinopathy, S25, S60–S62, S73 S70–S71
niacin, S53 revisions summary, S4 hospital care, S82
NICE-SUGAR trial, S81 screening, S10 hypoglycemia, S38
nonproliferative diabetic retinopathy statins, S72 insulin, S41
(NPDR), S61 prison, S87 pharmacological therapy, S41–S42
nursing home. see hospital care Professional Practice Committee, S3, pregnancy, S78–S79
S88–S89 progression estimates, S11
obstructive sleep apnea, S18 proliferative diabetic retinopathy, S61 retinopathy, S25, S60–S62, S73
older adults protein, S22, S23, S59 SMBG, S34
A1C levels, S9 psychosocial screening, care, S25–S26 statin therapy, S53
depression screening, S67 P2Y12 receptor antagonist, S55 testing, S11
diabetes complications screening, S67 type 2 diabetes
glycemic targets, S68 race/ethnicity, S9, S12, S35. see also African A1C goals, S35
hyperglycemia, S67, S68 Americans; Asian Americans A1C/macrovascular complications
hypertension, S67 RAS inhibitors, S51, S59 relationships, S36
care.diabetesjournals.org Index S93

children and adolescents, S12–S13, overview, S11 UK Prospective Diabetes Study (UKPDS),
S74 pharmacological therapy, S31–S32, S36, S59
classification, S8 S42–S46 ulcers, S63–S64
combination therapy, S42, S43 pregnancy, S78–S79
community screening, S12 prevention, delay of, vascular endothelial growth factor (VEGF),
comorbidities, S74 S31–S32 S61, S62
diagnosis, S11–S13 recommendations, S11, S31 vascular pathology measures, S37
diagnostic tests, S12 retinopathy, S25, S60–S62, S73 Veterans Affairs Diabetes Trial (VADT), S36
hypoglycemia, S38 risk factors, S11–S12 vildagliptin, S44
ketoacidosis, S11 screening, S12, S31
lifestyle modifications, S31, S42 testing interval, S12 weight loss, S21, S55